SOD Levels Research Articles

Pentagalloyl glucose enhanced the stress resistance to delay aging process in Caenorhabditis elegans

Aging is a complex biological process characterized by gradual and irreversible functional deterioration, strongly associated with oxidative stress. Pentagalloyl glucose (PGG) has attracted increasing attention due to its potent antioxidant and anti-stress properties. This study investigated the potential of PGG to mitigate the aging process under stress in RAW 264.7 cells and Caenorhabditis elegans models. The expression of vital genes associated with stress was also measured to explain the action mechanism of PGG in C. elegans. The findings showed that PGG supplementation not only significantly enhanced the stress tolerance of RAW 264.7 cells, but also prolonged lifespan and reduced the ROS and lipofuscin accumulation in C. elegans induced by stress. Meanwhile, the improvement effect of PGG on delaying aging development was also manifested in the protection of mitochondrial function and neuronal integrity. Moreover, daf-16 nuclear translocation and sod-3 expression were significantly enhanced by PGG to delay the aging process. Mechanistically, PGG might alleviate aging by improving daf-16, sod-3, ctl-1, and gst-4 levels in the DAF-16/FOXO pathway and upregulating skn-1 and gst-4 expression in the SKN-1/Nrf2 pathway. Our study provided novel insights into the role of PGG in combating stress-induced aging.

Hepatoprotective action mechanism and quantification of soyasaponin Bb in Abri Herba by HPLC and network pharmacology

Ethnopharmacological relevanceThe herb of Abrus cantoniensis Hance (AC) is an important Traditional Chinese Medicine (TCM) and is also used as an herbal tea with hepatoprotective action. Soyasaponin Bb is one of the pharmacodynamic substances of AC for the herb's effective pharmacological activity. This study aims to investigate the anti-fibrotic and hepatoprotective activities of soyasaponin Bb in vivo and in vitro experiments, mechanism by network pharmacology and quantification by HPLC. Materials and methodsHigh-performance liquid chromatography (HPLC) was applied to evaluate the quality of the herb and determine the contents of soyasaponin Bb from different sources and parts of the AC. In vivo experiments were conducted to induce an acute liver injury model by injecting CCl4 into mice, and an in vitro hepatic fibrosis model was established by cultivating LX-2 cells with TGF-β1. These models were used to explore the anti-fibrotic and hepatoprotective effects of soyasaponin Bb and its underlying mechanisms. In addition, the potential target genes corresponding to soyasaponin Bb were identified using the Swiss Target Prediction database through network pharmacology methods. Meanwhile, hepatic fibrosis targets were screened using the GeneCards, TTD, and OMIM disease databases. The STING database was used to construct the protein-protein interaction (PPI) network of soyasaponin Bb-hepatic fibrosis. The soyasaponin Bb-hepatic fibrosis disease target-pathway network was constructed using Cytoscape 3.9.1 software. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to enrich and analyze the common targets of the drug and the disease, aiming to identify the potential targets and pathways involved in the anti-fibrotic and hepatoprotective effects of soyasaponin Bb. ResultsThe content of soyasaponin Bb varied across different sources, with the roots containing the highest concentration, up to 0.2480%. In vivo experiments showed that soyasaponin Bb had a protective effect against CCl4-induced acute liver injury, effectively inhibiting the increase in ALT and AST levels and slowing down the hepatocyte inflammatory damage caused by CCl4. Soyasaponin Bb also down-regulated MDA levels and up-regulated SOD levels, indicating a certain antioxidant capacity. In vitro cell experiments showed that soyasaponin Bb could effectively inhibit the proliferation of HSC-LX2 cells induced by TGF-β1 by regulating the TGF-β1/α-SMA pathway, significantly down-regulate the protein expression of TGF-β1 and α-SMA, while also reducing the levels of inflammatory cytokines IL-6 and IL-1β. Further network pharmacology analysis suggested that soyasaponin Bb can exert anti-fibrosis activity by regulating the IBD signaling pathway, Th17 signaling pathway, Hepatitis B signaling pathway, and JAK-STAT signaling pathway. ConclusionSoyasaponin Bb is primarily distributed in the root of AC, and it has a strong protective effect against CCl4-induced acute liver injury. It can reduce the level of inflammatory factors, relieve inflammation, and exert anti-fibrotic activity by regulating the TGF-β1/α-SMA pathway. Its potential anti-hepatic fibrosis mechanism has been investigated through network pharmacology.

Relationship of SOD-1 Activity in Metabolic Syndrome and/or Frailty in Elderly Individuals.

Although aging is a natural phenomenon, in recent years it has accelerated. One key factor implicated in the aging process is oxidative stress. Oxidative stress also plays a role in frailty (frail) and metabolic syndrome (MetS). A total of 66 elderly persons (65 years old and older) with no acute or severe chronic disorders were assessed for waist circumference (WC), arterial blood pressure, glycemia, glycated hemoglobin (HbA1c), plasma lipids, and activity of erythrocyte superoxide dismutase (SOD-1). Patients were classified as NonMetS-Nonfrail (n = 19), NonMetS-frail (n = 20), MetS-Nonfrail (n = 17), or MetS-frail (n = 10). There were no significant differences in superoxide dismutase activity among investigated elderly groups. However, the data suggest that MetS individuals, both frail and nonfrail, have higher risk factors for cardiovascular disease compared to NonMetS individuals. The correlations analyses of SOD-1 and other metabolic indices suggest that SOD-1 levels may be influenced by age, total cholesterol, HDL cholesterol, and fasting glucose levels in certain groups of seniors. Aging is associated with decreased antioxidant enzyme SOD-1 activity with glucose alteration in frailty syndrome as well as with lipids disturbances in metabolic syndrome. These factors provide a nuanced view of how frailty and metabolic syndrome interact with various health parameters, informing both clinical practice and future research directions.

The impact of Codonopsis Pilosulae and Astragalus Membranaceus extract on growth performance, immunity function, antioxidant capacity and intestinal development of weaned piglets.

The objective of this study was to examine the impact of Codonopsis pilosula and Astragalus membranaceus extract (CA) on the growth performance, diarrhea rate, immune function, antioxidant capacity, gut microbiota, and short-chain fatty acids (SCFAs) in weaned piglets. A total of forty-eight 31-day-old weaned piglets, were divided into four groups randomly based on the treatment type: control group (CON), low dose group (LCA, 0.5% CA), medium dose group (MCA, 1.0% CA), and high dose group (HCA, 1.5% CA), and were fed for a duration of 28 days. On the morning of the 1st and 29th day, the piglets were assessed by weighing them on an empty stomach, recording their daily feed intake and diarrhea rate. CA increased the average daily weight gain and reduced F/G without significant differences, and the diarrhea rate was reduced in the LCA and MCA groups. Furthermore, the levels of T-AOC, SOD, GSH-Px, and MDA were increased. The levels of T-AOC in the LCA group and the MCA group, SOD in the MCA group, and GSH-Px in the HCA group were significantly higher compared with the CON group (p < 0.05). Additionally, CA significantly increased IgM, IgG, and IgA levels (p < 0.05). The results of gut microbiota analysis showed that the bacterial population and diversity of faeces were changed with the addition of CA to basal diets. CA increased the abundance of the beneficial bacterial Firmicutes and Lactobacillus. Additionally, Compared with the CON group, CA significantly increased the SCFAs content of weaned piglets (p < 0.05). CA can alleviate oxidative stress, improve immunity and antioxidant capacity, increase the abundance of beneficial bacteria, and the content of SCFAs for improving the intestinal barrier of piglets, thus promoting growth and reducing diarrhea rate in weaned piglets.

Polystyrene nanoplastics mediate skeletal toxicity through oxidative stress and the BMP pathway in zebrafish (Danio rerio)

The widespread presence of micro(nano)plastics (MNPs) has generated public concern. Studies have indicated that MNPs can accumulate in mammalian bones; however, research on the skeletal toxicity and underlying molecular mechanisms of MNPs in aquatic organisms remains limited. We subjected zebrafish embryos to three varying levels (1, 10, 100 μg/mL) of polystyrene nanoplastics (PSNPs) exposure over a period of 7 days in our research. The results revealed that PSNPs significantly reduced the body length and hatching rate of zebrafish, leading to skeletal deformities. mRNA level analysis showed significant upregulation of sp7, sparc, and smad1 genes transcription by PSNPs. Moreover, PSNPs markedly downregulated the mRNA levels associated with runx2a, bmp2a, and bmp4. Further investigations demonstrated that PSNPs dramatically increased ROS levels in zebrafish larvae, with significant downregulation of transcription levels of sod1 and cat genes, resulting in a sharp increase in transcription levels of apoptosis-related regulatory genes bcl-2 and bax. Furthermore, PSNPs led to a marked rise in Caspase 3 activity in zebrafish larvae, suggesting the initiation of apoptosis. PSNPs also notably inhibited alkaline phosphatase (AKP) activity. Compared to a 4-day exposure, a 7-day exposure to PSNPs intensified abnormalities across multiple indicators. In summary, our research indicates that PSNPs cause significant oxidative stress in zebrafish larvae, resulting in apoptosis. Moreover, PSNPs disrupt the transcription of genes related to skeletal development through the bone morphogenetic protein (BMP) pathway, further disrupting skeletal development processes and ultimately resulting in skeletal deformities in zebrafish larvae. This study provides new insights into the skeletal toxicity of MNPs.

Combined Toxic Effects and Mechanisms of Chloroacetic Acid and N-Nitrosodimethylamine on Submerged Macrophytes

Disinfection by-products (DBPs) such as chloroacetic acids (CAAs) and N-Nitrosodimethylamine (NDMA) are prevalent pollutants in surface waters, particularly with the increasing use of chlorine-based disinfectants. The entry of these DBPs into water bodies may increase accordingly, posing ecological risks to aquatic life. To assess the toxic effects of CAAs and NDMA on submerged macrophytes, Vallisneria natans was exposed to different concentrations of CAAs (1.0, 10.0, and 100.0 μg L−1) and NDMA (0.1, 1.0, and 10.0 μg L−1). A RI value of &lt;1 indicates that simultaneous exposure to CAAs and NDMA can produce an antagonistic effect. Both CAAs and NDMA adversely affect the photosynthetic system of plants. In the NDMA treatment group, chlorophyll a content decreases with increasing concentration, accounting for 96.03%, 60.80%, and 58.67% of the CT group, respectively. Additionally, it effectively triggers the plant’s antioxidant response, with significant increases in SOD, POD, and GSH levels. Among these, the combined treatment group AN2 (10 + 1 μg L−1) showed the most significant change in SOD activity, reaching 3.57 times that of the CT group. Ultrastructural changes also revealed stress responses in leaf cells and damage to organelles. Furthermore, metabolomics provided insights into the metabolic responses induced by CAAs or NDMA in V. natans leaves, where the composition and metabolism of lipids, fatty acids, cofactors and vitamins, amino acids, nucleotides, and some antioxidants were regulated, affecting plant growth. This study provides preliminary information for the ecological risk assessment of submerged plants by complex contamination with the disinfection by-products CAA and NDMA.

Baicalin enhances antioxidant, inflammatory defense, and microbial diversity of yellow catfish (Pelteobagrus fulvidraco) infected with Aeromonas hydrophila.

The aim of this research was to clarify the mechanism through which baicalin exerts its inhibitory effects on Aeromonas hydrophila infection. The antibacterial efficacy of baicalin was assessed by determining its minimum inhibitory concentration (MIC) against A. hydrophila. Various parameters, including the growth curve, cell wall integrity, biofilm formation, AKP content, and morphological alterations of A. hydrophila, were analyzed. In vivo experiments involved the administration of A. hydrophila 4 h postintraperitoneal injection of varying doses of baicalin to induce infection, with subsequent monitoring of mortality rates. After a 3 d period, liver, spleen, and intestinal tissues were harvested to evaluate organ indices, antioxidant and immune parameters, as well as intestinal microbial composition. The findings indicated that baicalin treatment resulted in the disruption of the cell wall of A. hydrophila, leading to the loss of its normal structural integrity. Furthermore, baicalin significantly inhibited biofilm formation and facilitated the release of intracellular proteins (P < 0.05). In vivo, baicalin enhanced the survival rates of yellow catfish infected with A. hydrophila. Compared to the control group, the liver index of yellow catfish was elevated, while the spleen and intestinal indices were reduced in the baicalin-treated group (P < 0.05). Additionally, baicalin at an appropriate dosage was found to increase levels of SOD, GSH, CAT, ACP, and AKP in yellow catfish (P < 0.05), while simultaneously decreasing MDA accumulation and the mRNA expression of inflammatory markers such as Keap1, IL1, IFN-γ, and TNF-α, (P < 0.05). Moreover, baicalin significantly enhanced the operational taxonomic unit (OTU) count in A. hydrophila-infected yellow catfish (P < 0.05), restoring the abundance of Barnesiellaceae, Enterobacteriaceae, Plesiomonas, and UBA1819 (P < 0.05). In summary, baicalin demonstrates the potential to improve the survival rate of yellow catfish subjected to A. hydrophila infection, augment antioxidant and immune responses, mitigate inflammation, and enhance intestinal microbial diversity.

Licorice Extract Isoliquiritigenin Protects Endothelial Function in Type 2 Diabetic Mice.

Endothelial dysfunction occurs prior to atherosclerosis, which is an independent predictor of cardiovascular diseases (CVDs). Diabetes mellitus impairs endothelial function by triggering oxidative stress and inflammation in vascular tissues. Isoliquiritigenin (ISL), one of the major bioactive ingredients extracted from licorice, has been reported to inhibit inflammation and oxidative stress. However, the therapeutic effects of ISL on ameliorating type 2 diabetes (T2D)-associated endothelial dysfunction remain unknown. In our animal study, db/db male mice were utilized as a model for T2D-associated endothelial dysfunction, while their counterpart, heterozygote db/m+ male mice, served as the control. Mouse brain microvascular endothelial cells (mBMECs) were used for in vitro experiments. Interleukin-1β (IL-1β) was used to induce endothelial cell dysfunction. ISL significantly reversed the impairment of endothelium-dependent relaxations (EDRs) in db/db mouse aortas. ISL treatment decreased ROS (reactive oxygen species) levels in db/db mice aortic sections and IL-1β-treated endothelial cells. Encouragingly, ISL attenuated the overexpression of pro-inflammatory factors MCP-1, TNF-α, and IL-6 in db/db mouse aortas and IL-1β-impaired endothelial cells. The NOX2 (NADPH oxidase 2) overexpression was inhibited by ISL treatment. Notably, ISL treatment restored the expression levels of IL-10, SOD1, Nrf2, and HO-1 in db/db mouse aortas and IL-1β-impaired endothelial cells. This study illustrates, for the first time, that ISL attenuates endothelial dysfunction in T2D mice, offering new insights into the pharmacological effects of ISL. Our findings demonstrate the potential of ISL as a promising therapeutic agent for the treatment of vascular diseases, paving the way for the further exploration of novel vascular therapies.

Evaluation of SOD and MDA levels with the Cytotoxicity of some Plant Extracts Toward Human Rhabdomyosarcoma Cell Lines

حظيت السمية الخلوية للمستخلصات النباتية باهتمام كبير في السنوات الأخيرة لتقييم نشاطها ضد الأورام. تركز الوقاية الكيميائية من السرطان على السمية الخلوية للمستخلصات النباتية لتكون سامة تجاه خطوط الخلايا السرطانية دون أن تؤثر على الخلايا الطبيعية. الهدف من هذه الدراسة هو تقييم السمية الخلوية لمستخلصي الزنجبيل و أوراق الزيتون ومزيجهما بنسبة 1: 1 تجاه خطوط خلايا RD وتقدير فعالية هذه المسخلصات ضد الاجهاد التاكسدي بدلالة SOD و MDA. تم الحصول على المستخلصات الكحولية لكل من الزنجبيل وأوراق الزيتون بطريقة السوكسيلت. وحضر المستخلص الثالث بخلط كميات متساوية من مستخلص أوراق الزيتون والزنجبيل بنسبة 1: 1. تم تحضير اطباق من خطوط الخلايا RD وخطوط الخلايا الاعتيادية وتم اختبار تراكيز مختلفة من المستخلصات المحضرة (12.5 - 800 ميكروغرام / مل) لتسجيل فعالياتهم تجاه كل من RD وخطوط الخلايا الطبيعية. . كذلك ، تم تقدير مستوى انزيم SOD و MDA اعتمادًا على طرائق العمل الخاصة بهما. اظهرت النتائج وجود فرق معنوي بين السمية الخلوية للتراكيز المدروسة لكل مستخلص تجاه خطوط الخلايا RD، اذ انخفضت قابلية بقاء خطوط الخلايا RD مع زيادة تراكيز المستخلصات ، وفي نفس الوقت لم تؤثر تلك المستخلصات على خطوط الخلايا الطبيعية. كذلك بينت النتائج ازدياد مستويات SOD مع زيادة تركيز المستخلص على عكس مستويات MDA التي انخفضت مع زيادة تراكيز المستخلص. يمكن الاستنتاج بان نشاط المستخلصات المحضرة تجاه خطوط الخلايا RD دون التأثير على خطوط الخلايا الطبيعية يعزز مبادئ المنع الكيميائي للسرطان ، إلى جانب الخصائص المضادة للأكسدة التي يمكن أن تقلل من الإجهاد التأكسدي الذي يصاحب الخلايا السرطانية وتنشيط العوامل الطبيعية المضادة للاكسدة في جسم الانسان.

Dynamic changes in Beclin-1, LC3B, and p62 in aldose reductase-knockout mice at different time points after ischemic stroke

Ischemic stroke is a brain injury caused by cerebral blood circulation disorders and is closely related to oxidative stress. Aldose reductase (AR) is a critical enzyme involved in oxidative stress. Autophagy has previously been found to play a key role in cerebral ischemia‒reperfusion injury. However, it is still unclear how autophagy molecules change after cerebral ischemia‒reperfusion injury in AR knockout mice (AR−/−). A transient middle cerebral artery occlusion (tMCAO) model was generated in AR−/− mice, and the neurological deficit scores of the mice were observed and recorded on Days 1, 3 and 5 after tMCAO. Neuronal damage in the ischemic penumbra was observed by TTC, HE, and Nissl staining. The expression of the autophagy-related molecules Beclin-1, LC3II/I, and P62 as well as that of molecules related to inflammation, oxidative stress, and neurological damage was detected by RT‒qPCR, western blotting, and immunofluorescence. Autophagosomes were observed using a transmission electron microscope. Cerebral ischemia‒reperfusion injury caused neurological deficits and ischemic infarction in tMCAO mice (P < 0.01). Beclin-1, Bcl2/Bax, SOD, GSH-px, P62, PSD95, and TOM20 levels decreased (P < 0.05), while IL-6, LC3II/I, and GFAP levels increased (P < 0.01) in the AR−/− tMCAO-1d group and the AR−/− tMCAO-3d group, compared to those in the sham group. Beclin-1, Bcl2/Bax, NOX4, GSH-px, P62, and PSD95 levels increased (P < 0.01), while IL-6, LC3II/I, and GFAP levels decreased (P < 0.01) in the AR−/− tMCAO-5d group compared to those in the AR−/− tMCAO-1d group. Autophagosome formation was observed in tMCAO mice. In summary, the changes in autophagy proteins in the brain tissue of the AR−/− mice after tMCAO were more obvious on Days 1 and 3 after tMCAO. The expression of Beclin-1 and P62 decreased, and the expression of LC3B increased after cerebral ischemia‒reperfusion injury in AR−/− mouse brain tissue.

Increased susceptibility of human limbal aniridia fibroblasts to oxidative stress

Aniridia-associated keratopathy originates from a haploinsufficiency of the transcription factor PAX6 (PAX6+/−). In the corneal epithelium of PAX6+/− mice, a significant increase in oxidized proteins was observed, accompanied by impaired compensation for elevated oxidative stress (OS). The extent to which limbal fibroblast cells (LFCs) are affected by an increased susceptibility to OS in cases of congenital aniridia (AN) has not been determined, yet. Our aim was to examine the impact of OS on antioxidant enzyme expression in normal and AN-LFCs. Following isolation and culture of primary LFCs (n = 8) and AN-LFCs (n = 8), cells were treated with cobalt chloride for 48 h to chemically induce hypoxic conditions and OS. Subsequently, HIF-1α/-2α, PHD1/2, Nrf2, CAT, SOD1, PRDX6, and GPX1 gene expression was examined by qPCR. SOD1, PRDX6, and GPX1 protein levels were assessed from the cell lysate by Western blot. The induction of hypoxia led to reduced HIF-1α gene expression in both fibroblast groups (p≤0.008), while the decrease in PHD1 was limited to AN-LFCs (p = 0.0007). On the other hand, under hypoxic conditions, PHD2 showed higher mRNA expression in AN-LFCs compared to normal LFCs (p = 0.013). As a result of OS, the mRNA levels of Nrf2 (p<0.0001) and the antioxidant enzymes CAT (p = 0.005), SOD1 (p = 0.005), GPX1 (p = 0.002) decreased in AN-LFCs. This was accompanied by an increased protein expression of SOD1 (p = 0.019) and PRDX6 (p=0.0009). In the normal LFC group, the induced extent of OS had no impact on the gene (p≥0.151) and protein expression (p ≥ 0.629) of antioxidant enzymes, except for the GPX1 mRNA level (p = 0.027). AN-LFCs exhibit higher susceptibility to OS than normal LFCs. Therefore, in AN-LFCs, there are sustained alterations in gene and protein expression of antioxidative enzymes even after 48 h of CoCl2 treatment.

Epicatechin ameliorates palmitate-induced insulin resistance in C2C12 myogenic cells by alleviating oxidative stress and activating the AMPK/ACC pathway

ABSTRACT Epicatechin (EC) is a water-soluble natural organic compound belonging to the flavanol class of compounds. It exhibits various physiological activities such as anti-inflammatory, antioxidant, treatment of mitochondrial diseases, and prevention of cardiovascular diseases.To examineEC’s impact and mechanism on adult myoblasts’ insulin resistance. The effects of various EC concentrations on the viability of C2C12 adult myoblasts were measured, as were glucose consumption and glycogen content; in vitro antioxidant activity of EC was measured; cellular oxidative marker content and apoptosis were measured; and protein expression was detected by Western blot. A model of insulin resistance in C2C12 myogenic cells was established using palmitic acid. EC significantly increased the glucose consumption and glycogen content; EC increased the levels of CAT, SOD and GSH and decreased the levels of NO, MDA and ROS; EC decreased the apoptosis rate of cells; EC treatment upregulated the levels of GLUT4, p-AMPK, p-ACC, NRF2, and HO-1 proteins. These results suggest that EC can regulate the NRF2/HO-1 signaling pathway, enhance GLUT4 transport, activate AMPK/ACC pathway, enhance cellular uptake of glucose, thus effectively improving insulin resistance in C2C12 cells.

Ursolic Acid Ameliorates Alcoholic Liver Injury through Attenuating Oxidative Stress-Mediated Ferroptosis and Modulating Gut Microbiota.

Ursolic acid (UA), a triterpenoid found in plants, has many health benefits for liver function. However, understanding how UA intervenes in alcohol-induced ferroptosis remains unclear because of the lack of research. This study explored the protective effects of UA on alcohol-induced liver injury and further elucidated its mechanism of action. Using a mouse model, acute liver injury was induced via high-dose alcohol gavage, and UA's protective effects were assessed by analyzing serum and liver indicators. The results indicated that UA has a significant protective effect against alcohol-induced liver injury in mice. UA significantly decreased serum ALT, AST, TC, and TG levels. Histopathological examination revealed that UA significantly ameliorated liver damage. UA increased ADH, ALDH, and CYP2E1 enzyme expression levels and alleviated alcohol-induced oxidative damage by regulating alcohol metabolism. Moreover, UA increased SOD and GSH-Px levels and lowered the MDA levels in the liver. Furthermore, UA regulated ACC expression by activating the LKB1/AMPK pathway, thereby inhibiting lipid synthesis and peroxidation. UA also upregulated the expression of GPX4 and SLC7A11 in the liver and exerted hepatoprotective effects by inhibiting alcohol-induced ferroptosis. Additionally, 16S rRNA amplicon sequencing showed that excessive alcohol consumption significantly affected the composition of the mouse gut microbiota, with UA intervention proving to be beneficial for improving gut microbiota imbalance. We also validated the protective effects of UA on alcohol-treated HepG2 cells at the cellular level. In summary, these results revealed that UA can alleviate alcoholic liver injury by inhibiting oxidative stress-mediated ferroptosis and regulating gut microbiota. These findings suggest that UA may serve as a functional component in the prevention of alcoholic liver disease.

Effect of drought stress on the growth, ovary development, antioxidant capacity, sex hormone content, and reproductive-related gene expression of red swamp crayfish (Procambarus clarkii)

Hainan Province is located in the southernmost part of China. Natural conditions, such as high temperature, drought, and typhoons, have become important factors restricting the development of the red swamp crayfish (Procambarus clarkii) industry. This study aimed to examine the effects of drought stress on growth, ovarian development, antioxidant capacity, sex hormone content, and reproductive gene expression of P. clarkii. An annual survey was conducted on the ovarian development of female P. clarkii in Hainan Province, China, from January 2023 to January 2024. Under the influence of drought and prolonged light, the ovaries of P. clarkii entered the stage of rapid development in May, and the maturity was the highest in September, reaching a maximum of 2.88. In this study, female P. clarkii with a body weight of 31.09 ± 1.20 g were randomly divided into 5 groups with 6 replicates per group for drought stress experiment at 0 d (control group), 10 d, 20 d, 30 d, and 40 d, respectively. Compared with the control group, the maturity of P. clarkii was significantly improved after 10 d, 30 d, and 40 d of stress. The levels of GSH-Px, SOD, and T-AOC in hepatopancreas and hemolymph were significantly decreased after 30 d of drought, and MDA level was significantly increased after 10 d, 20 d, and 30 d of drought treatment. The contents of E, PROG, 17A-OHP, and E2 in the hemolymph of female P. clarkii were significantly decreased after more than 30 d of drought stress. Cyclin B mRNA transcription level decreased significantly after 20 d of drought. The expression levels of vgr and cdc2 significantly increased after 30 d and 40 d of drought, while foxL2 significantly decreased and pcna significantly increased after 40 d of drought. Based on the above results, 30 d drought was the most effective in promoting the ovarian development of female P. clarkii.

Clinical effect of anti-resistance exercise combined with nutritional intervention in the treatment of elderly patients with sarcopenia.

This study aims to evaluate the efficacy of a combined intervention involving resistance exercise and nutritional support in improving grip strength, walking speed, and skeletal muscle density among elderly individuals suffering from sarcopenia. Data from a cohort of 500 elderly sarcopenic patients were segregated into observation and control cohorts based on distinct treatment modalities. Baseline evaluations included weight, grip strength, walking speed, and skeletal muscle density. Changes in these parameters and oxidative stress markers were monitored and compared at 1-, 3-, and 6-month intervals. Baseline grip strength for the observation and control groups stood at (20.25 ± 2.34) and (21.06 ± 2.97) kg, respectively. Walking speed was measured at (0.99 ± 0.12) and (0.98 ± 0.20) m/s, respectively. Skeletal muscle density registered (42.98 ± 4.17) and (42.77 ± 5.02) Hu for the observation and control groups, respectively, while muscle mass index was recorded as (6.19 ± 1.46) and (6.20 ± 1.68) kg/m2, respectively. Limb skeletal muscle mass for both cohorts was (16.83 ± 3.57) and (16.77 ± 3.89) kg. No significant disparities were discerned in baseline characteristics between the groups. Following 1, 3, and 6 months, the observation group exhibited marked enhancements in grip strength and walking speed (P < .05), with substantially superior grip strength compared to the control cohort (P < .05). Notably, skeletal muscle density, muscle mass index, and limb skeletal muscle mass exhibited significant augmentation in the observation group (P < .05), while no significant alterations were observed in the control cohort. Oxidative stress-related parameters displayed no notable differences between groups pretreatment (P > .05). Post-treatment, levels of Hcy, IFN-γ, and MDA markedly decreased in both groups, with considerably lower levels evident in the observation cohort (P < .05). Moreover, SOD levels exhibited significant post-treatment increments in both groups, with markedly higher levels observed in the observation group (P < .05). An integrated approach of resistance exercise and nutritional support significantly enhances grip strength, walking speed, and skeletal muscle density in elderly patients with sarcopenia, contributing to better prognoses and improved quality of life.

Association of MnSOD, CAT, and GPx1 Gene Polymorphism with Risk of Diabetic Nephropathy in South Indian Patients: A Case-Control Study.

Diabetic nephropathy (DN) is one of the common complications of type 2 diabetes mellitus (T2DM), and oxidative stress plays a key role in the pathogenesis of DN. Studies have demonstrated that antioxidants (MnSOD, CAT, and GPx1) may reduce the complications associated with T2DM. The purpose of the study is to correlate the role of antioxidant gene polymorphisms in the pathogenesis of DN among T2DM individuals in the South Indian population. It clarifies the importance of early manifestation and reliable genetic indicators modulating the oxidative stress mechanism in DN.The study participants were divided and grouped as Group 1: Control, Group 2: T2DM without DN, and Group 3: T2DM with DN (n = 100 in each group). The levels of plasma glucose, HbA1c, renal profile, SOD, CAT, GPx1, MDA, and TAS were assessed. MnSOD (rs4880), CAT (rs1049982), and GPx1 (rs1050450) polymorphisms were genotyped via Tetra-arms PCR.The genotypes of GPx1 depict a significant role in the progression of DN in T2DM patients (co-dominant [OR: 2.134; 95% CI (1.202-3.788), p < 0.01], dominant [OR: 2.015; 95% CI (1.117-3.634), p = 0.02], and recessive model [OR: 2.215; 95% CI (1.235-3.972), p = 0.008]); whereas rs4880 and rs1049982 polymorphisms are not associated with DN progression. As a result, GPx1 (rs1050450) polymorphism could be a diagnostic risk factor for developing DN in T2DM patients. Moreover, the genotypes of rs4880 and rs1049982 polymorphism show significant difference in the antioxidant parameters compared to the genotypes of rs1050450.In contradiction to earlier studies, the current study demonstrates that the genotypes of rs1050450 (GPx1) can be considered as an influential component for higher susceptibility and risk of developing DN in T2DM patients among the South Indian population.

Impact of Extremely Low-Frequency Electromagnetic Fields on Skeletal Muscle of Sedentary Adult Mice: A Pilot Study.

Extremely low-frequency electromagnetic fields (ELF-EMFs) are ubiquitous in industrialized environments due to the continuous use of electrical devices. Our previous studies demonstrated that ELF-EMFs affect muscle cells by modulating oxidative stress and enhancing myogenesis. This pilot study investigated these effects on the skeletal muscles of sedentary adult mice, assessing physiological responses to ELF-EMF exposure and potential modulation by antioxidant supplementation. Male C57BL/6 mice were exposed to ELF-EMFs (0.1 or 1.0 mT) for 1 h/day for up to 5 weeks and fed a standard diet without or with N-acetyl-cysteine (NAC). The results showed transient increases in muscle strength (after 2 weeks of exposure at 1.0 mT), potentially linked to muscle fiber recruitment and activation, revealed by higher PAX7 and myosin heavy chain (MyH) expression levels. After ELF-EMF exposure, oxidative status assessment revealed transient increases in the expression levels of SOD1 and catalase enzymes, in total antioxidant capacity, and in protein carbonyl levels, markers of oxidative damage. These effects were partially reduced by NAC. In conclusion, ELF-EMF exposure affects skeletal muscle physiology and NAC supplementation partially mitigates these effects, highlighting the complex interactions between ELF-EMFs and antioxidant pathways in vivo. Further investigations on ELF-EMFs as a therapeutic modality for muscle health are necessary.

Minocycline alleviates lipopolysaccharide-induced cardiotoxicity by suppressing the NLRP3/Caspase-1 signaling pathway.

Minocycline (Min), as an antibiotic, possesses various beneficial properties such as anti-inflammatory, antioxidant, and anti-apoptotic effects. Despite these known qualities, the precise cardioprotective effect and mechanism of Min in protecting against sepsis-induced cardiotoxicity (SIC) remain unspecified. To address this, our study sought to assess the protective effects of Min on the heart. Lipopolysaccharide (LPS) was utilized to establish a cardiotoxicity model both in vivo and in vitro. Min was pretreated in the models. In the in vivo setting, evaluation of heart tissue histopathological injury was performed using hematoxylin and eosin (H&E) staining and TUNEL. Immunohistochemistry (IHC) was employed to evaluate the expression levels of NLRP3 and Caspase-1 in the heart tissue of mice. During in vitro experiments, the viability of H9c2 cells was gauged utilizing the CCK8 assay kit. Intracellular ROS levels in H9c2 cells were quantified using a ROS assay kit. Both in vitro and in vivo settings were subjected to measurement of oxidative stress indexes, encompassing glutathione (GSH), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. Additionglly, myocardial injury markers like lactate dehydrogenase (LDH) and creatine kinase MB (CK-MB) activity were quantified using appropriate assay kits. Western blotting (WB) analysis was conducted to detect the expression levels of NOD-like receptor protein-3 (NLRP3), caspase-1, IL-18, and IL-1β, alongside apoptosis-related proteins such as Bcl-2 and Bax, and antioxidant proteins including superoxide dismutase-1 (SOD-1) and antioxidant proteins including superoxide dismutase-1 (SOD-2), both in H9c2 cells and mouse heart tissues. In vivo, Min was effective in reducing LPS-induced inflammation in cardiac tissue, preventing cell damage and apoptosis in cardiomyocytes. The levels of LDH and CK-MB were significantly reduced with Min treatment. In vitro studies showed that Min improved the viability of H9C2 cells, reduced apoptosis, and decreased ROS levels in these cells. Further analysis indicated that Min decreased the protein levels of NLRP3, Caspase-1, IL-18, and IL-1β, while increasing the levels of SOD-1 and SOD-2 both in vivo and in vitro. Min alleviates LPS-induced SIC by suppressing the NLRP3/Caspase-1 signalling pathway in vivo and in vitro.

Paternal zinc deficiency alters offspring metabolic status in Drosophila melanogaster

BackgroundThis study delves into the understudied yet potentially crucial role of paternal zinc deficiency in programming offspring metabolic outcomes. By examining paternal zinc deficiency, we aim to shed light on a previously unexplored avenue with the potential to significantly impact future generations. We investigated the intergenerational effects of paternal zinc deficiency on metabolic parameters in Drosophila melanogaster. MethodsDietary zinc deficiency was induced by supplementing the diet of Drosophila F0 male flies with TPEN (N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine) from egg stage. The F0 male flies after eclosion were mated with age-matched virgin female flies from the control group, resulting in the F1 offspring generation. The F1 generation were then cultured on a standard diet for subsequent metabolic analyses, including assessments of body weight, locomotion, and levels of glucose, trehalose, glycogen, and triglycerides as well as the expression of related genes. ResultsWe observed an increase (p<0.05) in body weight in male parent flies and female offspring. Negative geotaxis performance was also impaired in the female offspring. Paternal zinc deficiency exerted distinct effects on carbohydrate and lipid metabolism, as evidenced by a significant (p<0.05) increase in trehalose and triglyceride levels in both parent and offspring. Additionally, zinc deficiency led to alterations in the expression of key metabolic genes, including significant (p<0.05) increase in DILP2 mRNA levels, highlighting potential links to insulin signaling. Also, there were reduced mRNA levels of SOD1 and CAT in both parental and offspring generations. Parental zinc deficiency also increased the expression of Eiger and UPD2 mRNA in the offspring, suggesting potential perturbations in the immune response system. ConclusionThese findings underscore the link between zinc status and various physiological and molecular processes, revealing both immediate and intergenerational impacts on metabolic, antioxidant, and inflammatory pathways and providing valuable insights on the implications of paternal zinc deficiency in Drosophila melanogaster.

PEI/MMNs@LNA-542 nanoparticles alleviate ICU-acquired weakness through targeted autophagy inhibition and mitochondrial protection.

Intensive care unit-acquired weakness (ICU-AW) is prevalent in critical care, with limited treatment options. Certain microRNAs, like miR-542, are highly expressed in ICU-AW patients. This study investigates the regulatory role and mechanisms of miR-542 in ICU-AW and explores the clinical potential of miR-542 inhibitors. ICU-AW models were established in C57BL/6 mice through cecal ligation and puncture (CLP) and in mouse C2C12 myoblasts through TNF-α treatment. In vivo experiments demonstrated decreased muscle strength, muscle fiber atrophy, widened intercellular spaces, and increased miR-542-3p/5p expression in ICU-AW mice model. In vitro experiments indicated suppressed ATG5, ATG7 and LC3II/I, elevated MDA and ROS levels, decreased SOD levels, and reduced MMP in the model group. Similar to animal experiments, the expression of miR-542-3p/5p was upregulated. Gel electrophoresis explored the binding of polyethyleneimine/mesoporous silica nanoparticles (PEI/MMNs) to locked nucleic acid (LNA) miR-542 inhibitor (LNA-542). PEI/MMNs@LNA-542 with positive charge (3.03 ± 0.363 mV) and narrow size (206.94 ± 6.19 nm) were characterized. Immunofluorescence indicated significant internalization with no apparent cytotoxicity. Biological activity, examined through intraperitoneal injection, showed that PEI/MMNs@LNA-542 alleviated muscle strength decline, restored fiber damage, and recovered mitochondrial injury in mice. In conclusion, PEI/MMNs nanoparticles effectively delivered LNA-542, targeting ATG5 to inhibit autophagy and alleviate mitochondrial damage, thereby improving ICU-AW.