Enhanced Superoxide Dismutase Activity Research Articles

Genomic insights and functional evaluation of Lacticaseibacillus paracasei EG005: a promising probiotic with enhanced antioxidant activity.

Probiotics, such as Lacticaseibacillus paracasei EG005, are gaining attention for their health benefits, particularly in reducing oxidative stress. The goal of this study was to reinforce the antioxidant capacity of EG005, along with comprehensive genomic analysis, with a focus on assessing superoxide dismutase (SOD) activity, acid resistance and bile tolerance, and safety. EG005 was screened for SOD activity and change of SOD activity was tested under various pH conditions. Its survival rates were assessed in acidic (pH 2.5) and bile salt (0.3%) conditions and the antibiotic MIC test and hemolysis test were performed to evaluate safety. Genetic analyses including functional identification and phylogenetic tree construction were performed. The SOD overexpression system was constructed using Ptuf, Pldh1, Plhd2, and Pldh3 strong promoters. EG005 demonstrated higher SOD activity compared to Lacticaseibacillus rhamnosus GG, with optimal activity at pH 7.0. It showed significant acid and bile tolerance, with survival rates recovering to 100% after 3 h in acidic conditions. Phylogenetic analysis confirmed that EG005 is closely related to other L. paracasei strains with ANI values above 98%. Overexpression of SOD using the Ptuf promoter resulted in a two-fold increase in activity compared to the controls. Additionally, EG005 exhibited no hemolytic activity and showed antibiotic susceptibility within safe limits. Our findings highlight EG005's potential as a probiotic with robust antioxidant activity and high tolerance to gastrointestinal conditions. Its unique genetic profile and enhanced SOD activity through strong promoter support its application in probiotic therapies and functional foods. Further research should be investigated to find the in vivo effects of EG005 on gut health and oxidative stress reduction. In addition, attB and attP-based recombination, combined with CRISPR-Cas9 technologies, could offer a more stable alternative for long-term sodA gene expression in commercial and medical applications.

Sodium transport and redox regulation in Saccharomyces cerevisiae under osmotic stress depending on oxygen availability

This study explores the molecular mechanisms behind the differential responses of Saccharomyces cerevisiae industrial strains (ATCC 9804 and ATCC 13007) to osmotic stress. We observed that, in contrast to ATCC 9804 strain, sodium flux in ATCC 13,007 is not N, N’-dicyclohexylcarbodiimide (DCCD)-sensitive under osmotic stress, suggesting a distinct ion homeostasis mechanism. Under aerobic conditions, osmotic stress increased reduced SH groups by 45% in ATCC 9804 and 34% in ATCC 13,007. In contrast, under microaerophilic conditions, both strains experienced a 50% reduction in thiol groups. Notably, ATCC 13,007 exhibited a 1.5-fold increase in catalase (CAT) activity under aerobic stress compared to standard conditions, while ATCC 9804 showed enhanced CAT activity due to SH group binding. Additionally, superoxide dismutase (SOD) activity was doubled during aerobic growth in both strains, with ATCC 13,007 showing a 1.5-fold higher SOD activity under osmotic stress. The results demonstrate that S. cerevisiae adapts to osmotic stress differently under aerobic and microaerophilic conditions, with aerobic conditions promoting Pma-Ena-Trk interplay, reduced thiol levels and increased catalase activity, while microaerophilic conditions demonstrate Pma-Nha-Trk interplay and shifts redox balance towards oxidized thiol groups and enhance superoxide dismutase activity. Understanding these mechanisms can aid in developing stress-resistant yeast strains for industrial applications.

Nootkatone mitigates periodontal inflammation and reduces alveolar bone loss via Nrf2/HO-1 and NF-κB pathways in rat model of periodontitis.

Periodontitis (PD) is a chronic inflammatory disease leading to alveolar bone loss. This study investigated the effect of nootkatone and regulatory mechanism in reducing periodontal inflammation and alveolar bone loss in a rat model. Twenty male Sprague-Dawley rats were divided into control, periodontitis, and nootkatone-treated groups (45 or 90 mg/kg). Ligature induction method was adopted to establish the PD model. After 21 days, rats received daily gavage of either saline or nootkatone for 10 days. Alveolar bone loss was assessed using micro-CT. Histological analyses included hematoxylin and eosin (H&E), tartrate-resistant acid phosphatase (TRAP), and Masson's trichrome stainings. Immunohistochemistry for heme oxygenase 1 (HO-1) and nuclear factor erythroid-2 related factor 2 (Nrf2) were performed in periodontal tissues. Content of inflammatory cytokines IL-1β, IL-6, and TNF-α in gingival tissues around ligature were assessed using ELISA kits. Malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were analyzed and Western blot for NF-κB expression in gingival tissues were performed. Nootkatone significantly reduced the distance from cementoenamel junction to alveolar bone crest (CEJ-ABC), enhanced bone mineral density (BMD), bone volume (BV), and BV/total volume (TV) ratio in ligature-induced rats. Higher dose of nootkatone (90 mg/kg) did not show more significant therapeutic effect than lower dose (45 mg/kg). Histological staining showed decreased osteoclasts' number and improved bone architecture in the nootkatone group. Content of IL-1β, IL-6, and TNF-α and inflammatory cell infiltration level in gingival tissues around the ligature were decreased in the nootkatone-treatment rats. Nootkatone increased Nrf2 and HO-1 protein expression and decreased NF-κB protein level, suppressing MDA levels and enhancing SOD activity. In a rat model, nootkatone effectively mitigates periodontal inflammation and alveolar bone loss through the Nrf2/HO-1 and NF-κB pathways. These findings suggest nootkatone as a promising therapeutic agent for the treatment of periodontitis.

Protective effect and mechanism of lycium barbarum polysaccharide against UVB-induced skin photoaging.

Cellular senescence can be categorized into two main types, including exogenous and endogenous aging. Photoaging, which is aging induced by ultraviolet (UV) radiation, significantly contributes to exogenous aging, accounting for approximately 80% of such cases. Superoxide Dismutase (SOD) is a class of antioxidant enzymes, with SOD2 being predominantly localized in the mitochondrial matrix. Ultraviolet radiation (UVR) inhibits SOD2 activity by acetylating the key lysine residues on SOD2. Sirtuin3 (SIRT3), the principal mitochondrial deacetylase, enhances the anti-oxidant capacity of SOD2 by deacetylating. Lycium barbarum polysaccharide (LBP) is the main bioactive component extracted from Lycium barbarum (LB). It has been reported to have numerous potential health benefits, such as anti-oxidation, anti-aging, anti-inflammatory and anti-apoptotic properties. Furthermore, LBP has been shown to regulate hepatic oxidative stress via the SIRT3-SOD2 pathway. The aim of this study was to construct a UVB-Stress-induced Premature Senescence (UVB-SIPS) model to investigate the protective effects and underlying mechanisms of LBP against UVB-induced skin photoaging. Irradiated with different UVB doses to select the suitable dose for constructing the UVB-SIPS model. Cell morphology was observed using a microscope. The proportion of senescent cells was assessed by senescence-associated β-galactosidase (SA-β-gal) staining. Cell viability was studied using the Cell Counting Kit-8 (CCK-8). Intracellular levels of reactive oxygen species (ROS) were observed using flow cytometry and an inverted fluorescence microscope. Expression of γ-H2AX was investigated using flow cytometry. Western blot (WB) was used to verify the expression of senescence-associated proteins (p21, p53, MMP-1, and MMP-3). Enzyme-Linked Immunosorbnent Assay (ELISA) was used to measure pro-inflammatory cytokines levels (IL-6, TNF-α). WB was also used to analyze the expression of SIRT3, SOD2, and Ac-SOD2, and a specific kit was employed to detect SOD2 activity. Our results suggested that the UVB-SIPS group pre-treated with LBP exhibited a reduced proportion of cells positive for SA-β-gal staining, mitigated production of intracellular ROS, an amelioration in γ-H2AX expression, and down-regulated expression of senescence-associated proteins and pro-inflammatory cytokines as compared to the UVB-SIPS group. Moreover, in contrast to the control group, the UVB-SIPS group showed regulated SIRT3 expression and SOD activity, elevated Ac-SOD2 expression and an increased ratio of Ac-SOD2/SOD2. However, the UVB-SIPS group pre-treated with LBP showed an upregulation of SIRT3 expression and enhanced SOD activity, a reduction in AC-SOD2 expression, and a decreased ratio of AC-SOD2/SOD2, compared to the untreated UVB-SIPS group. Additionally, the photo-protective effect of LBP was diminished following treatment with 3-TYP, a SIRT3-specific inhibitor. This study suggested that LBP, a natural component, exhibits anti-oxidant and anti-photoaging properties, potentially mediated through the SIRT3-SOD2 pathway.

Mitigation of lipopolysaccharide-induced intestinal injury in rats by Chimonanthus nitens Oliv. essential oil via suppression of mitochondrial fusion protein mitofusin 2 (MFN2)-mediated mitochondrial-associated endoplasmic reticulum membranes (MAMs) formation

Ethnopharmacological relevanceChimonanthus nitens Oliv. is a traditional Chinese medicine with anti-inflammatory and antioxidant properties that has commonly been used for colds, fevers, and other diseases. However, its role and specific mechanism in sepsis-associated intestinal injury have not been reported. Aim of the studyC. nitens Oliv. essential oil (CEO), an organic active compound extracted from the traditional Chinese medicine C. nitens Oliv. exhibits notable anti-inflammatory and antioxidant properties. Nevertheless, the therapeutic potential of CEO for septic intestinal injury remains undocumented. This study thus aims to elucidate the anti-inflammatory and antioxidant effects of CEO in the context of acute intestinal injury and to investigate its mechanisms of action in septic rats. Materials and methodsCell and animal models were established using LPS to investigate the impact of CEO on LPS-induced intestinal pathological injury and the secretion of inflammatory factor IL-1β. The effects of CEO on the expression of NLRP3, caspase-1, and MFN2, p-p65 protein were also examined, as well as its influence on oxidative stress injury and mitochondrial-associated endoplasmic reticulum membrane (MAM) formation. Generation of an MFN2 knockout IEC-6 cell line allowed comprehensive investigation of the protective mechanism of CEO. ResultsIn rat models, CEO reduced IL-1β secretion, inhibited caspase-1, ZO-1 expression and NF-κB p65 phosphorylation, while also decreasing malondialdehyde levels and enhancing superoxide dismutase activity in intestinal tissues. Cellular experiments demonstrated its ability to decrease IL-1β secretion; NLRP3, caspase-1, and MFN2 expression; NF-κB p65 phosphorylation; reactive oxygen species (ROS) production, and mitochondrial dysfunction. MFN2 knockdown enhanced these effects synergistically with CEO, indicating potential therapeutic synergy. Further, MFN2 knockdown significantly mitigated LPS-induced NLRP3 and caspase-1 expression, IL-1β secretion, ROS production, NF-κB p65 phosphorylation and MMP reduction in IEC-6 cells, while inhibiting MAM formation and NLRP3 localization on MAMs. Importantly, MFN2 downregulation and CEO synergistically reduced LPS-induced IL-1β secretion and ROS production while inhibiting MAM formation in IEC-6 cells, thus inhibiting NLRP3 inflammasome activation. ConclusionCEO mitigates inflammation and oxidative stress by inhibiting MAM formation and is thus a promising intervention for septic intestinal injury.

Acute and prolonged effects of Bacillus amyloliquefaciens GF424-derived SOD on antioxidant defense in healthy individuals challenged with intense aerobic exercise

Reactive oxygen species (ROS) play a vital role in cellular functions but can lead to oxidative stress and contribute to degenerative diseases when produced in excess. Maintaining redox balance is essential and can be achieved through innate defense mechanisms or external antioxidants. Superoxide dismutase (SOD) is a key enzyme that mitigates intracellular oxidative stress by converting harmful free radicals into hydrogen peroxide, which is subsequently neutralized by catalase and glutathione peroxidase. Previous studies have demonstrated the antioxidant capabilities of SOD derived from Bacillus amyloquefaciens GF424 (BA-SOD) in murine models exposed to either irradiation or SOD1 gene deletion. In this study, a randomized clinical trial was conducted to evaluate the antioxidative benefits of BA-SOD in healthy individuals undergoing acute aerobic exercise (AAE). Eighty participants were randomly assigned to receive either BA-SOD or a placebo for 8 weeks. Antioxidant enzyme activities and glutathione levels were measured before, immediately after, and 30 min post-exercise. A single dose of BA-SOD significantly reduced ROS levels induced by AAE, primarily by enhancing SOD activity in erythrocytes and activating glutathione peroxidase. Continuous BA-SOD administration was associated with a sustained increase in catalase activity and elevated levels of reduced glutathione (GSH). Transcriptomic and metabolomic analyses revealed that a single BA-SOD dose facilitated GSH oxidation, as evidenced by decreased levels of serine, glutamine, and glycine, and increased pyroglutamate levels. Additionally, repeated dosing led to increased expression of genes encoding isocitrate dehydrogenase and malic enzyme, which are involved in NADPH synthesis, as well as nicotinamide phosphoribosyl transferase and NAD kinase, which are essential for NADP availability–critical for converting oxidized glutathione (GSSG) back to GSH. These molecular insights align with clinical observations, suggesting that both acute and long-term BA-SOD supplementation may effectively enhance antioxidant defenses and maintain redox balance under oxidative stress conditions.

Rutin Ameliorates Inflammation and Oxidative Stress in Ulcerative Colitis by Inhibiting NLRP3 Inflammasome Signaling Pathway.

Ulcerative colitis (UC) is an idiopathic inflammatory disease. We intend to explore the mechanism of Rutin in the therapy of UC. Disease activity index (DAI) and hematoxylin-eosin staining were employed to assess therapeutic effect of Rutin on dextran sulfate sodium-stimulated mice. The proliferation was detected by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide assay. Oxidative stress (OS) was assessed by measuring reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD). Inflammatory factors were detected using enzyme-linked immunosorbent assay and immunofluorescence staining. mRNA and protein expressions were detected by real-time quantitative polymerase chain reaction and immunoblotting assay. Rutin decreased DAI scores and ameliorated pathological damage in UC mice with decreased levels of inflammatory factors. Rutin recovered the inhibited proliferation of fetal human colon cells caused by lipopolysaccharide. Rutin inhibited OS by reducing ROS and MDA, while enhancing SOD activity in LPS-induced fetal human colon cells. Rutin inhibited NLRP3 inflammasome in UC mice and cell model. Silencing NLRP3 enhanced the inhibitory effect of Rutin on OS in lipopolysaccharide-induced fetal human colon cells. Conversely, NLRP3 overexpression reversed the restraining role of Rutin in OS. Rutin ameliorates UC by inhibiting inflammation and OS through suppressing NLRP3 inflammasome.

Protium heptaphyllum essential oil from the fruit as a sedative and anesthetic in Rhamdia quelen: influence in cardiac frequency, biochemical, and oxidative parameters.

This study aimed to evaluate the effects of Protium heptaphyllum fruit essential oil (PHEO) on the physiology of silver catfish (Rhamdia quelen) during anesthesia and recovery, through studying echocardiograms, oxidative status, and metabolic parameters. Three experiments were performed: (1) 50 silver catfish juveniles were submitted to anesthesia and recovery tests with 300, 400, 500, 600, and 700mg L-1 of PHEO. (2) Echocardiogram analysis was performed in anesthetized and non-anesthetized fish. (3) Biochemical parameters were evaluated at 0, 30, 60, and 120min of recovery after being anesthetized for 3min with 600mg L-1 PHEO. Times to sedation and deep anesthesia were reduced with PHEO increasing concentrations. The echocardiogram showed a higher cardiac rate in anesthetized fish. Plasma glucose levels increased in control fish through recovery time, but anesthetized fish showed lower levels than controls at 120min of recovery. Metabolic parameters such as plasma and hepatic glucose did not show changes considering the recovery time of up to 120min. Hepatic glycogen, lactate, and triglycerides reduced their levels over recovery times. Fish anesthetized enhanced superoxide dismutase activity and thiobarbituric acid reactive substances levels but decreased reduced glutathione (GSH) levels at 30min compared to controls. After 60min, GSH values were significantly higher in anesthetized fish than in controls. These results suggest that PHEO at 600mg L-1 is an effective anesthetic for the rapid handling of silver catfish, providing stable metabolic parameters and enhanced antioxidant responses during recovery. Echocardiogram analysis confirms the anesthetic effect, supporting PHEO as a viable and efficient option for fish anesthesia in aquaculture. The use of PHEO in aquaculture can enhance fish welfare by reducing stress during handling and transportation, potentially leading to improved growth, health, and survival rates.

Antioxidative effect of astragalosides on acute pancreatitis in mice.

The research examined the antioxidative impact of astragalosides (AST) on experimental acute pancreatitis (AP) in mice. This study aims to assess the correlation between varying doses of astragalosides and superoxide dismutase (SOD) activity in an acute pancreatitis mouse model. By examining the interplay between astragaloside's protective effects and its antioxidant properties, we aim to deepen our understanding of its therapeutic potential in acute pancreatitis. The AP model in mice was induced by retrograde injection of sodium deoxycholate into the biliary and pancreatic ducts. Serum amylase activity was monitored at various time points following induction. Furthermore, 24 hours post-induction, levels of serum nitric oxide (NO), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) content in pancreatic tissue were assessed. The findings of this study illustrated that AST, while exhibiting a protective effect in experimental AP, could effectively lower the elevated serum NO levels, reduce MDA production, and enhance SOD activity in model mice. AST notably reduced MDA levels in the pancreatic tissue of AP mice, underscoring its ability to inhibit membrane peroxidation induced by oxygen free radicals. Furthermore, AST was observed to elevate SOD activity in scavenging oxygen free radicals in pancreatic tissue. These findings suggest that AST enhances recovery in an experimental acute pancreatitis mouse model by exerting antioxidative effects.

Repeated Sulforaphane Treatment Reverses Depressive-like Behavior and Exerts Antioxidant Effects in the Olfactory Bulbectomy Model in Mice.

Growing evidence suggests that activators of nuclear factor erythroid-derived 2-like 2 (Nrf2), such as sulforaphane, may represent promising novel pharmacological targets for conditions related to oxidative stress, including depressive disorder. Therefore, we conducted a study to explore the behavioral and biochemical effects of repeated (14 days) sulforaphane (SFN) treatment in the olfactory bulbectomy (OB) animal model of depression. An open field test (OFT), splash test (ST), and spontaneous locomotor activity test (LA) were used to assess changes in depressive-like behavior and the potential antidepressant-like activity of SFN. The OB model induced hyperactivity in mice during the OFT and LA as well as a temporary loss of self-care and motivation in the ST. The repeated administration of SFN (10 mg/kg) effectively reversed these behavioral changes in OB mice across all tests. Additionally, a biochemical analysis revealed that SFN (10 mg/kg) increased the total antioxidant capacity in the frontal cortex and serum of the OB model. Furthermore, SFN (10 mg/kg) significantly enhanced superoxide dismutase activity in the serum of OB mice. Overall, the present study is the first to demonstrate the antidepressant-like effects of repeated SFN (10 mg/kg) treatment in the OB model and indicates that these benefits may be linked to improved oxidative status.

Therapeutic Potential of Pentoxifylline in Paraquat-Induced Pulmonary Toxicity: Role of the Phosphodiesterase Enzymes.

Pentoxifylline (PTX), a non-selective phosphodiesterase inhibitor, has demonstrated protective effects against lung injury in animal models. Given the significance of pulmonary toxicity resulting from paraquat (PQ) exposure, the present investigation was designed to explore the impact of PTX on PQ-induced pulmonary oxidative impairment in male mice.Following preliminary studies, thirty-six mice were divided into six groups. Group 1 received normal saline, group 2 received a single dose of PQ (20 mg/kg; i.p.), and group 3 received PTX (100 mg/kg/day; i.p.). Additionally, treatment groups 4-6 were received various doses of PTX (25, 50, and 100 mg/kg/day; respectively) one hour after a single dose of PQ. After 72 hours, the animals were sacrificed, and lung tissue was collected.PQ administration caused a significant decrease in hematocrit and an increase in blood potassium levels. Moreover, a notable increase was found in the lipid peroxidation (LPO), nitric oxide (NO), and myeloperoxidase (MPO) levels, along with a notable decrease in total thiol (TTM) and total antioxidant capacity (TAC) contents, catalase (CAT) and superoxide dismutase (SOD) enzymes activity in lung tissue. PTX demonstrated the ability to improve hematocrit levels; enhance SOD activity and TTM content; and decrease MPO activity, LPO and NO levels in PQ-induced pulmonary toxicity. Furthermore, these findings were well-correlated with the observed lung histopathological changes.In conclusion, our results suggest that the high dose of PTX may ameliorate lung injury by improving the oxidant/antioxidant balance in animals exposed to PQ.

Rosa roxburghii Fruit Extracts Upregulate Telomerase Activity and Ameliorate Cell Replicative Senescence.

Anti-aging functional foods benefit the elderly. Telomeres are chromosomal ends that maintain genome stability extended by telomerase catalytic subunit TERT. Due to the end-replication problem, telomeres shorten after each cell cycle without telomerase in most human cells, and eventually the cell enters the senescence stage. Natural products can attenuate the aging process by increasing telomerase activity, such as TA-65. However, TA-65 is expensive. Other Chinese natural products may achieve comparable effects. Here, we found that Rosa roxburghii fruit extracts effectively increase TERT expression and telomerase activity in cultured human mesenchymal stem cells. Both R. roxburghii fruit extracts obtained by freeze-drying and spray-drying increased the activity of telomerase. R. roxburghii fruit extracts were able to reduce reactive oxygen species levels, enhance superoxide dismutase activity, and reduce DNA damage caused by oxidative stress or radiation. R. roxburghii fruit extracts promoted cell proliferation, improved senescent cell morphology, delayed replicative cellular senescence, attenuated cell cycle suppressors, and alleviated the senescence-associated secretory phenotype. Transcriptome and metabolic profiling revealed that R. roxburghii fruit extracts promote DNA replication and telomere maintenance pathways and decrease triglyceride levels. Overall, we provide a theoretical basis for the application of R. roxburghii fruit as an anti-aging product.

Xanthine oxidoreductase inhibition ameliorates high glucose-induced glomerular endothelial injury by activating AMPK through the purine salvage pathway

Xanthine oxidoreductase (XOR) contributes to reactive oxygen species production. We investigated the cytoprotective mechanisms of XOR inhibition against high glucose (HG)-induced glomerular endothelial injury, which involves activation of the AMP-activated protein kinase (AMPK). Human glomerular endothelial cells (GECs) exposed to HG were subjected to febuxostat treatment for 48 h and the expressions of AMPK and its associated signaling pathways were evaluated. HG-treated GECs were increased xanthine oxidase/xanthine dehydrogenase levels and decreased intracellular AMP/ATP ratio, and these effects were reversed by febuxostat treatment. Febuxostat enhanced the phosphorylation of AMPK, the activation of peroxisome proliferator-activated receptor (PPAR)-gamma coactivator (PGC)-1α and PPAR-α and suppressed the phosphorylation of forkhead box O (FoxO)3a in HG-treated GECs. Febuxostat also decreased nicotinamide adenine dinucleotide phosphate oxidase (Nox)1, Nox2, and Nox4 expressions; enhanced superoxide dismutase activity; and decreased malondialdehyde levels in HG-treated GECs. The knockdown of AMPK inhibited PGC-1α–FoxO3a signaling and negated the antioxidant effects of febuxostat in HG-treated GECs. Despite febuxostat administration, the knockdown of hypoxanthine phosphoribosyl transferase 1 (HPRT1) also inhibited AMPK–PGC-1α–FoxO3a in HG-treated GECs. XOR inhibition alleviates oxidative stress by activating AMPK–PGC-1α–FoxO3a signaling through the HPRT1-dependent purine salvage pathway in GECs exposed to HG conditions.

Unlocking renal Restoration: Mesaconine from Aconitum plants restore mitochondrial function to halt cell apoptosis in acute kidney injury

Acute kidney injury (AKI) is characterized by a sudden decline in renal function. Traditional Chinese medicine has employed Fuzi for kidney diseases; however, concerns about neurotoxicity and cardiotoxicity have constrained its clinical use. This study explored mesaconine, derived from processed Fuzi, as a promising low-toxicity alternative for AKI treatment. In this study, we assessed the protective effects of mesaconine in gentamicin (GM)-induced NRK-52E cells and AKI rat models in vitro and in vivo, respectively. Mesaconine promotes the proliferation of damaged NRK-52E cells and down-regulates intracellular transforming growth factor β1 (TGF-β1) and kidney injury molecule 1 (KIM-1) to promote renal cell repair. Concurrently, mesaconine restored mitochondrial morphology and permeability transition pores, reversed the decrease in mitochondrial membrane potential, mitigated mitochondrial dysfunction, decreased ATP production, inhibited inflammatory factor release, and reduced early apoptosis rates. In vivo, GM-induced AKI rat models exhibited elevated AKI biomarkers, in which mesaconine was effectively reduced, indicating improved renal function. Mesaconine enhanced superoxide dismutase activity, reduced malondialdehyde content, alleviated inflammatory infiltrate, mitigated tubular and glomerular lesions, and downregulated NF-κB (nuclear factor-κb) p65 expression, leading to decreased tumor necrosis factor-α (TNF-α) and IL-1β (interleukin-1β) levels in GM-induced AKI animals. Furthermore, mesaconine inhibited the expression of renal pro-apoptotic proteins (Bax, cytochrome c, cleaved-caspase 9, and cleaved-caspase 3) and induced the release of the anti-apoptotic protein bcl-2, further suppressing apoptosis. This study highlighted the therapeutic potential of mesaconine in GM-induced AKI. Its multifaceted mechanisms, including the restoration of mitochondrial dysfunction, anti-inflammatory and antioxidant effects, and apoptosis mitigation, make mesaconine a promising candidate for further exploration in AKI management.

Carboxymethylated Rhizoma alismatis polysaccharides reduces the risk of calcium oxalate stone formation by reducing cellular inflammation and oxidative stress.

This study aims to elucidate the mechanism and potential of Rhizoma alismatis polysaccharides (RAPs) in preventing oxidative damage to human renal proximal tubule epithelial cells. The experimental approach involved incubating HK-2 cells with 100nm calcium oxalate monohydrate for 24h to establish a cellular injury model. Protection was provided by RAPs with varying carboxyl group contents: 3.57%, 7.79%, 10.84%, and 15.33%. The safeguarding effect of RAPs was evaluated by analyzing relevant cellular biochemical indicators.Findings demonstrate that RAPs exhibit notable antioxidative properties. They effectively diminish the release of reactive oxygen species, lactate dehydrogenase, and malondialdehyde, a lipid oxidation byproduct. Moreover, RAPs enhance superoxide dismutase activity and mitochondrial membrane potential while attenuating the permeability of the mitochondrial permeability transition pore. Additionally, RAPs significantly reduce levels of inflammatory factors, including NLRP3, TNF-α, IL-6, and NO. This reduction corresponds to the inhibition of overproduced pro-inflammatory mediator nitric oxide and the caspase 3 enzyme, leading to a reduction in cellular apoptosis. RAPs also display the ability to suppress the expression of the HK-2 cell surface adhesion molecule CD44.The observed results collectively underscore the substantial anti-inflammatory and anti-apoptotic potential of all four RAPs. Moreover, their capacity to modulate the expression of cell surface adhesion molecules highlights their potential in inhibiting the formation of kidney stones. Notably, RAP3, boasting the highest carboxyl group content, emerges as the most potent agent in this regard.

Evaluation of In Vitro and In Vivo Antioxidant Potential of the Ethyl Acetate Fraction of Cyperus Pangorei Rhizome

Background and Aim: Antioxidants derived from natural sources, particularly those rich in flavonoids and phenolic compounds, have attracted considerable interest for their potential health benefits in combating oxidative stress-related diseases. This study aimed to evaluate the antioxidant potential of the ethyl acetate (EtAc) fraction obtained from Cyperus pangorei rhizome, focusing on both in vitro and in vivo assessments. Methods: The EtAc fraction was subjected to RP-HPLC analysis to identify and quantify phenolic compounds and flavonoids. Acute toxicity testing was performed to assess the safety profile of the EtAc fraction. In vitro antioxidant activity was determined using DPPH and ABTS+ radical scavenging assays. In vivo evaluation of antioxidant activity was conducted in Triton X-100-induced oxidative stress model in mice, measuring malondialdehyde (MDA) content, glutathione (GSH) levels, and superoxide dismutase (SOD) activity in liver tissues. Results: RP-HPLC analysis confirmed the presence of quercetin, luteolin, and apigenin in the EtAc fraction. The fraction exhibited significant dose-dependent antioxidant activity in both DPPH and ABTS+ assays, with IC50 values indicating potent scavenging effects. In the Triton X-100-induced stress model, administration of the EtAc fraction led to a reduction in MDA levels, restoration of GSH levels, and enhancement of SOD activity in mouse liver tissues. Conclusion: The findings suggest that the EtAc fraction from C. pangorei possesses promising antioxidant properties, as evidenced by its ability to mitigate oxidative stress-related damage both in vitro and in vivo.

A Novel Tetrapeptide Ala-Phe-Phe-Pro (AFFP) Derived from Antarctic Krill Prevents Scopolamine-Induced Memory Disorder by Balancing Lipid Metabolism of Mice Hippocampus.

Memory impairment is a serious problem with organismal aging and increased social pressure. The tetrapeptide Ala-Phe-Phe-Pro (AFFP) is a synthetic analogue of Antarctic krill derived from the memory-improving Antarctic krill peptide Ser-Ser-Asp-Ala-Phe-Phe-Pro-Phe-Arg (SSDAFFPFR) after digestion and absorption. The objective of this research was to assess the neuroprotective effects of AFFP by reducing oxidative stress and controlling lipid metabolism in the brains of mice with memory impairment caused by scopolamine. The 1H Nuclear magnetic resonance spectroscopy results showed that AFFP had three active hydrogen sites that could contribute to its antioxidant properties. The findings from in vivo tests demonstrated that AFFP greatly enhanced the mice's behavioral performance in the passive avoidance, novel object recognition, and eight-arm maze experiments. AFFP reduced oxidative stress by enhancing superoxide dismutase activity and malondialdehyde levels in mice serum, thereby decreasing reactive oxygen species level in the mice hippocampus. In addition, AFFP increased the unsaturated lipid content to balance the unsaturated lipid level against the neurotoxicity of the mice hippocampus. Our findings suggest that AFFP emerges as a potential dietary intervention for the prevention of memory impairment disorders.

Foliar application of phenylalanine, tryptophan, and tyrosine in fragrant rice production: Aroma, yield, grain quality, and economic return

Phenylalanine, tryptophan, and tyrosine are amino acids that are important to the growth and development of crops. However, the application of these amino acids in fragrant rice (Oryza sativa L.) production has not been reported. The present study aimed to investigate the effects of exogenous amino acids on aroma, yield, grain quality, and economic return of fragrant rice. At the heading stage, phenylalanine, tryptophan, and tyrosine at 0.50, 1.00, and 2.00 g L−1 were foliar applied to fragrant rice plants respectively and the treatment sprayed with distilled water was taken as control. The results showed that the foliar application of these amino acids significantly increased grain yield and seed-setting rate of fragrant rice. The total return and net income of fragrant rice production increased due to amino acids and the highest or equally highest net income and benefit-cost ratio was recorded in phenylalanine treatments with 0.50 and 1.00 g L−1 and tryptophan with 1.00 g L−1. However, amino acids applied at 2.00 g L−1 significantly decreased the benefit-cost ratio. Foliar application of phenylalanine, tryptophan, and tyrosine significantly enhanced superoxide dismutase activity. Phenylalanine treatments also increased the chlorophyll content. Compared with control, phenylalanine and tryptophan treatments significantly increased the grain content of 2-acetyl-1-pyrroline (2-AP) which is the key volatile component of fragrant rice aroma. The increased 2-AP content was explained by enhanced activity of proline dehydrogenase which plays an important part in catalyzing the conversion from proline to 2-AP. In conclusion, foliar application of phenylalanine, tryptophan, and tyrosine improved yield formation and economic return of fragrant rice. Foliar application of phenylalanine and tryptophan also enhanced 2-AP biosynthesis in fragrant rice.

Mitigating cyclophosphamide-associated gonadotoxicity in male Wistar rats: exploring the therapeutic potential of hesperidin.

Hesperidin, a bioactive flavanone glycoside prevalent in citrus fruits, with remarkable therapeutic properties stands out as a formidable defender against the debilitating reproductive toxicity associated with Cyclophosphamide (CYP) chemotherapy. This study explores the protective potential of hesperidin (HSP@100 mg/kg b.wt PO daily) against CYP-induced (@ 40 mg/kg b.wt IP once in a week) reproductive toxicity in male Wistar rats as several studies were documented on single dose toxicity of CYP. In this experiment, we chose multidosage drug effects, which are more relevant in chemotherapy. Twenty-four rats were divided into four groups: Group 1 (Control), group 2 (CYP-treated), group 3 (HSP-treated), and group 4 (CYP + HSP-treated) for 28 days. The experimental design included assessments of relative testicular weight, semen analysis, testosterone levels, oxidative stress markers, inflammatory cytokines, gross and histopathological changes, and immunohistochemical evaluation. The results revealed that the administration of CYP led to a significant reduction in testicular weight, sperm count, motility, and testosterone levels, accompanied by increased oxidative stress and inflammatory response. Hesperidin co-administration demonstrated a protective effect by restoring these parameters to near-normal levels. Histopathological analysis revealed improved testicular architecture in the group 4 compared with the group 2. Oxidative stress indices indicated that hesperidin attenuated CYP-induced damage by reducing malondialdehyde levels, enhancing superoxide dismutase activity and maintaining glutathione levels. Similarly, inflammatory cytokine analysis demonstrated anti-inflammatory effects of hesperidin by reducing tumor necrosis factor-alpha (TNF-α) and elevating interleukin-10 (IL-10) levels in the group 4. Immunohistochemical evaluation of nuclear factor-kappa B (NF-κB) revealed increased inflammation in the CYP group, while hesperidin significantly reduced NF-κB expression, suggesting its anti-inflammatory properties.

Efficacy of tanshinone IIA in rat models with myocardial ischemia-reperfusion injury: a systematic mini-review and meta-analysis.

Myocardial ischemia-reperfusion injury (MIRI) refers to severe damage to the ischemic myocardium following the restoration of blood flow, and it is a major complication of reperfusion therapy for myocardial infarction. Notably, drugs such as metoprolol have been utilized to reduce ischemia-reperfusion injury. Tanshinone IIA is a major constituent extracted from Salvia miltiorrhiza Bunge. Recently, tanshinone IIA has been studied extensively in animal models for controlling MIRI. Therefore, we conducted a meta-analysis on the application of tanshinone IIA in rat models with MIRI to evaluate the therapeutic effects of tanshinone IIA. A comprehensive search was conducted across PubMed, Web of Science, Embase, the Cochrane Library, the China National Knowledge Infrastructure database, the Wanfang database, and the Chinese Scientific Journal Database to gather studies on tanshinone IIA intervention in rat models with MIRI.We employed SYRCLE's risk of bias tool to assess study quality. The primary outcome indicators were superoxide dismutase (SOD) and malondialdehyde (MDA). Myocardial infarction area was a secondary outcome indicator. This study was registered at PROSPERO (registration number CRD 42022344447). According to the inclusion and exclusion criteria, 15 eligible studies were selected from 295 initially identified studies. In rat models with MIRI, tanshinone IIA significantly increased SOD levels while reducing MDA levels and myocardial infarction area. Moreover, the duration of myocardial ischemia influenced the effectiveness of tanshinone IIA. However, additional high-quality research studies are needed to establish the efficacy and definitive guidelines for the use of tanshinone IIA. Animal studies demonstrated that tanshinone IIA exerted a significant therapeutic effect when the ischemia duration was less than 40 minutes. Tanshinone IIA was found to be more effective when administered via intravenous, intraperitoneal, and intragastric routes at doses above 5 mg/kg. Additionally, treatment with tanshinone IIA at all stages-prior to myocardial ischemia, after ischemia but before reperfusion, prior to ischemia and after reperfusion, and after reperfusion-showed satisfactory results. Tanshinone IIA enhanced SOD activity and reduced MDA levels, thereby ameliorating oxidative stress damage during MIRI. Additionally, it reduced the myocardial infarction area, indicating its effectiveness in mitigating MIRI-induced damage in rats and demonstrating a myocardial protective effect. These findings contribute valuable insights for developing MIRI treatment strategies.