Reduced Malondialdehyde Levels Research Articles

Dual Role of Low Frequency Magnetic Field on Neuroinflammation Induced Dendritic Trimming And Memory Impairment on Rat Model of Sporadic Alzheimer’s Disease

AbstractBackgroundGliosis and dendritic loss is reported to be secondary to the amyloid beta (Aß) and hyperphosphorylated tau (hp‐tau) production in Alzheimer’s disease(AD) brain. STZ administration is reported to induce sporadic AD. Previous clinical or preclinical studies on effect of rTMS treatment in AD patients or APP23 mice showed cognitive improvement alone or as adjuvant therapy along‐with amelioration of the glial aggravation in the hippocampus. However, studies on the effect of magnetic field stimulation on the gliosis related dendritic trimming in animal models of sporadic AD is elusive. Therefore, in the present study we have looked in to the effect of extremely low frequency magnetic field stimulation (ELF‐MF; 17.96µT, 50Hz, 2hr/day) for one month post‐injection of STZ (bilateral, 3mg/kg).MethodTotal 45 animals were (ethical no. 937/IAEC/2016) randomly divided into five groups: Control, Sham, AD, Sham+MF and AD+MF. After assessing retention of spatial and avoidance memory using Morris water maze and passive avoidance step down test on 30th day, animals were sacrificed and tissues processed for oxidative stress and immunofluorescence, Golgi‐Cox staining.ResultBehavioural analysis revealed spatial memory improvement with no effect on the avoidance memory loss in AD+MF group as compared to AD group. We also found significant decrease in superoxide dismutase, catalase, GSH and increase in malon‐di‐aldehyde (MDA) in AD group. ELF‐MF treatment only reduced MDA level in hippocampus and frontal cortex. GFAP, IBA‐1 and hp‐tau (ser356) positive cells were found to be reduced in AD+MF group, as compared to all groups except Control. Sholl analysis revealed partial improvement of reduction in the number of intersection, bifurcation and length in basal and apical dendrite in the AD group after ELF‐MF treatment in CA3 layer. Convex hull analysis revealed a contradictory result showing reduction in apical (p = 0.018) and increase in basal dendrite (p = 0.038) of AD group as compared to control.ConclusionThese findings suggests dual role of ELF‐MF exposure on STZ model of AD showing improvement of spatial memory by reducing the gliosis induced dendritic loss but loss in avoidance memory.

Elucidation on potential utilization of Forsythia suspensa fruits in freshwater bivalve (Hyriopsis cumingii) culture against Aeromonas veronii infection

Plant extracts have been implicated in biological studies for their antibacterial, antioxidant, and anti-inflammatory properties. The curative efficacy of fruit extracts (Forsythia suspensa and Prunus mume) and three common antibiotics against Aeromonas veronii (alone or in extract-antibiotic combination) were clarified in vitro by microplate assays and checkerboard methods. Then the extracts with high antibacterial activity (F. suspensa) in vitro were exposed to Hyriopsis cumingii with A. veronii infection for in vivo assessments of their protective efficacy. Subsequently, oxidative stress markers, immune enzymes, and mRNA expression of immune genes in H. cumingii were investigated. Finally, principal component analysis of the physiological biomarkers and genetic markers that respond to A. veronii infection and extract exposures was conducted. The FICI values in vitro implied the following: P. mume combined with cephalexin was antagonistic, as opposed to other combinations whose effects were commutative or indifferent. In vivo results demonstrated that A. veronii caused lipid oxidative damage led to significant decreases in antioxidant defenses and induced immune responses in H. cumingii. F. suspensa significantly enhanced alanine transaminase activities and reduced malondialdehyde levels caused by A. veronii infection in gills and hepatopancreas. It also promoted antioxidant defenses, including superoxide dismutase activities and peroxidase contents, inhibiting increased alkaline phosphatase and acid phosphatase activities. Notably, 0.6% of F. suspensa extract (dry fruits: wet H. cumingii, w/w) reversed the upregulation of glutathione S-transferase and small heat shock protein mRNA levels in hepatopancreas and remarkably improved the survival rate of H. cumingii after the infection. Building on the research, F. suspensa may represent a promising substitute for offering effective protection to H. cumingii against bacterial diseases and contribute to the transformation and upgrading of the freshwater pearl culture industry.

Quercus coccinea Münchh leaves polyphenols: Appraisal acute lung injury induced by lipopolysaccharide in mice

Genus Quercus is a well-known source for its polyphenolic content and important biological activity. Plants belonging to the Quercus genus were traditionally used in asthma, inflammatory diseases, wound healing, acute diarrhea, and hemorrhoid. Our work intended to study the polyphenolic profile of the Q. coccinea (QC) leaves and to assess the protective activity of its 80% aqueous methanol extract (AME) against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Together, the potential molecular mechanism was investigated. Nineteen polyphenolic compounds (1–18), including tannins, flavone, and flavonol glycosides. Phenolic acids and aglycones were purified and identified from the AME of QC leaves. Treatment with AME of QC showed an anti-inflammatory effect evidenced by a remarkable decline in the count of white blood cells and neutrophils which was in harmony with decreasing the levels of high mobility group box-1, nuclear factor kappa B, tumor necrosis factor-α, and interleukin 1 beta. In addition, the antioxidant activity of QC was documented through the significant reduction in malondialdehyde level and elevation of reduced glutathione level and superoxide dismutase activity. Furthermore, the mechanism involved in the pulmonary protective effect of QC involved the downregulation of the TLR4/MyD88 pathway. The AME of QC showed a protective effect against LPS-induced ALI through the powerful anti-inflammatory and antioxidant activities which are linked to its abundancy with polyphenols.

Effects of ginseng consumption on the biomarkers of oxidative stress: A systematic review and meta-analysis.

Oxidative stress (OS) is a key factor involved in the initiation and development of chronic diseases. Despite its widespread acceptance as an antioxidant, the effects of ginseng on OS in human clinical trials have not been comprehensively analyzed. Therefore, this study aimed to synthesize the results of previous randomized clinical trials (RCTs) examining the impact of ginseng consumption on OS indicators. PubMed, Web of Science, Scopus, and Cochrane databases were searched for articles on the effects of ginseng consumption on oxidative stress markers up to March 20, 2023. Standardized mean difference (SMD) and 95% confidence intervals (CIs) were used to assess effect sizes. Twelve RCTs with 15 effect sizes revealed that the effects of ginseng lowered serum malondialdehyde (MDA) levels (SMD = 0.45, 95% CI: -0.87, -0.08; p = 0.03) and significantly increased the serum total antioxidant capacity (TAC) (SMD = 0.23, 95% CI: 0.01, 0.45; p = 0.04), oxidative dismutase (SOD) (SMD = 0.39, 95% CI: 0.21, 0.57; p < 0.0001), glutathione (GSH) (SMD = 0.36; 95% CI: 0.11, 0.61; p = 0.005), and glutathione reductase (GR) (SMD = 0.56; 95% CI: 0.31, 0.81; p < 0.0001) levels compared to the effects of placebo. However, the effects on serum glutathione peroxidase (GPx) and catalase (CAT) were not significant. Moreover, subgroup analysis based on intervention duration showed that ginseng consumption increased GPx (SMD = 0.91, 95% CI: 0.05, 1.78; p = 0.039) and CAT (SMD = 0.74, 95% CI: 0.27, 1.21; p = 0.002) levels after more than 4 weeks of intervention. According to the results of this meta-analysis, ginseng supplementation dramatically reduced MDA levels and increased TAC, SOD, GSH, and GR levels. Our results open up a new line of defense against oxidative stress-induced diseases.

A Na+/H+ antiporter-encoding salt overly sensitive 1 gene, LpSOS1, involved in positively regulating the salt tolerance in Lilium pumilum

Lilium pumilum has a strong salt tolerance. However, the molecular mechanism underlying its salt tolerance remains unexplored. Here, LpSOS1 was cloned from L. pumilum and found to be significantly enriched at high NaCl concentrations (100 mM). In tobacco epidermal cells, localization analysis showed that the LpSOS1 protein was primarily located in the plasma membrane. Overexpression of LpSOS1 resulted in up-regulation of salt stress tolerance in Arabidopsis, as indicated by reduced malondialdehyde levels and Na+/K+ ratio, and increased activity of antioxidant reductases (including superoxide dismutase, peroxidase, and catalase). Treatment with NaCl resulted in improved growth, as evidenced by increased biomass, root length, and lateral root growth, in both sos1 mutant (atsos1) and wild-type (WT) Arabidopsis plants that overexpressed LpSOS1, Under NaCl treatment,atsos1 and WT Arabidopsis plants overexpressing LpSOS1 exhibited better growth, with higher biomass, root length, and lateral root quantity, whereas in the absence of LpSOS1 overexpression, the plants of both lines were wilted and chlorotic and even died under salt stress. When exposed to salt stress, the expression of stress-related genes was notably upregulated in the LpSOS1 overexpression line of Arabidopsis as compared to the WT. Our findings indicate that LpSOS1 enhances salt tolerance in plants by regulating ion homeostasis, reducing Na+/K+ ratio, thereby protecting the plasma membrane from oxidative damage caused by salt stress, and enhancing the activity of antioxidant enzymes. Therefore, the increased salt tolerance conferred by LpSOS1 in plants makes it a potential bioresource for breeding salt-tolerant crops. Further investigation into the mechanisms underlying lily’s resistance to salt stress would be advantageous and could serve as a foundation for future molecular improvements.

The Effect of Liprotide-Encapsulated Vitamin D3 on MDA and SOD in Rats Deficient Vitamin D and Calcium

Background: Vitamin D deficiency is frequently correlated with elevated malondialdehyde (MDA) levels and decreased superoxide dismutase (SOD) activity. Several studies have demonstrated that vitamin D3 can reverse intracellular oxidative stress. However, vitamin D is prone to deterioration and instability. Liprotides contain lipids and proteins that can prevent vitamin D from oxidating.Objective: This study aims to investigate the effects of liprotide-encapsulated vitamin D3 on MDA concentrations and SOD activity in calcium and vitamin D-deficient rat models.Methods: The experimental post-test-only control group study used 24 Wistar rats randomly in 4 groups. Groups K(-), K(+), and P were fed a vitamin D and calcium-depleted AIN-93M diet for 14 days. Standard feed AIN-93M was received by normal groups (KN). Groups K- were deficient rats in vitamin D and calcium without intervention. The groups of K+ and P were given vitamin D3 (180 IU) which was non-encapsulated and liprotide-encapsulated for 28 days.The SOD activity was quantified with Superoxide Dismutase (SOD) Activity Assay Kit, while MDA levels were determined using Thiobarbituric Acid Reactive Substance (TBARS) method. The statistical analysis used One-way ANOVA test with Least Significant Difference follow-up test.Results: The MDA levels and SOD activity in the K+ and P groups had significant differences (p&lt;0.05) against the control group. Liprotides-encapsulated vitamin D3 significantly reduced MDA levels and enhanced SOD activity compared to non-encapsulated in rats with a deficiency in vitamin D and calcium.Conclusion: Liprotide-encapsulated vitamin D3 has the potential to increase SOD activity and decrease MDA levels.

Clemizole hydrochloride, a potent TRPC5 calcium channel inhibitor, prevents cisplatin-induced nephrotoxicity in Spraque-Dawley rats.

Cis-diamminedichloroplatinum (II) (cisplatin, Cis) is widely employed to treat several types of cancer. It has many important toxic side effects; one of the most important of which is nephrotoxicity. Clemizole hydrochloride (Clem) as the most potent inhibitor of TRPC5 channels was tested in an animal model of Cis-induced nephrotoxicity. Rats were divided into the following groups: control;Cis (8 mg/kg);Cis + 1 mg/kg Clem; Cis + 5 mg/kg Clem; Cis + 10 mg/kg Clem. Kidney injury was detected by histopathological and biochemical analysis. Urine urea nitrogen (UUN), creatinine, urine neutrophil gelatinase-associated lipocalin (NGAL), serum catalase (CAT), and malondialdehyde (MDA) levels were determined by enzyme-linked immunosorbent assay. Total antioxidant status (TAS) and total oxidant status (TOS)were studied using a colorimetric assay. Nephrin, synaptopodin, and Rac family small GTPase 1(RAC1) expressions were detected by Western blot analysis. Cis was found to induce histopathological alterations, including tubular degeneration, congestion, hemorrhage, hyaline casts, glomerular collapse, and apoptotic cell death. Clem at a doseof 1 and 5 mg/kgattenuated histopathological alterations. UUN, creatinine, and NGAL levels increased in the Cis-administered group, while all doses of Clem decreased in those. CAT and TAS levels decreased, whileTOS and oxidative stress index levels increased in the Cis-treated group. A dose of 1 and 5 mg Clemshowed antioxidant effects against oxidative stress. Cis induced lipid peroxidation by increasing MDA levels. All doses of Clem reduced MDA levels. Nephrin and synaptopodin expressions were decreased by Cis, and all doses of Clem increased that. All doses of Clem successfully depressed RAC1 expression. Clem showed a highly ameliorating effect on toxicity caused by Cis by blocking TRPC5 calcium channels.

Hepatoprotective Effect of Alpinetin on Thioacetamide-Induced Liver Fibrosis in Sprague Dawley Rat

Alpinetin is an original medicinal plant flavonoid derived from Alpinia katsumadai and has several biological activities. The current research aimed to evaluate the hepatoprotective effects of Alpinetin against thioacetamide (TAA)-induced liver cirrhosis in rats. Five groups of rats were utilized in this study. Hepatic injury was measured macroscopically and microscopically for entire groups. The rats’ body weight was significantly lower in the TAA control group, likened to rats fed with Silymarin or Alpinetin groups, while liver weight was significantly greater in the TAA control group when equated to rats nourished with Alpinetin groups. A histopathological investigation of hepatic tissues displayed that TAA remarkably induced hepatocyte necrosis and gristly connective tissue propagation in the TAA control group. Alpinetin implicitly decreased the influence of TAA toxicity and diminished fibrosis of liver tissues. The TAA control group presented an increase in liver enzymes (ALP, ALT, and AST) and a decrease in total protein and albumin. Rats who were fed Alpinetin had significantly lower hepatic enzyme activity as well as augmented total protein and albumin, yet they were close to the normal range. Superoxide dismutase (SOD) and Catalase (CAT) enzymes in hepatic homogenate were significantly reduced, and malondialdehyde (MDA) was meaningfully elevated in the TAA control group, while rats fed with Alpinetin had significantly increased SOD and CAT achievement and depressed MDA level. Alpinetin-gavaged groups had reduced levels of Tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6), significantly down-regulated Proliferating cell nuclear antigen (PCNA), Alpha-smooth muscle (α-SMA), and reduced hepatic stellate cell activity. However, the TAA control group significantly up-regulated PCNA and α-SMA and increased the activity of hepatic stellate cells. Alpinetin was nontoxic and could improve defensive mechanisms against hepatic tissue injury. Acute toxicity tests discovered no evidence of any toxic signs or dead rats, which highlights the safety of Alpinetin. Consequently, the investigation´s outcomes revealed that the hepatoprotective effects of Alpinetin in TAA-induced hepatic impairment might be due to reduced TAA toxicity, increased protein and albumin, increased SOD and CAT levels, reduced MDA levels, and modulation of inflammatory cytokines and their anti-oxidant activities, and suppressed PCNA and α-SMA.

Pengaruh Esktrak Daun Krokot (Portulaca oleracea) Terhadap Kadar Malonialdehide (MDA) Pada Tikus Yang Diinduksi Aloksan

Background: Diabetes mellitus is a degenerative disease caused by the pancreas being damaged in production or insulin cannot work effectively. Portulaca Oleracea Leaf Extract can help reduce levels of Malondialdehyde. The purpose of this study was to analyze the effect of Portulaca Oleracea leaf extract on malondialdehyde levels in alloxan-induced rats as a diabetes model.Methods: There were 30 rats in this study divided into 5 groups, each group consisting of 6 rats. The negative control group was only given aquadest and standard rat feed, the positive group was induced with alloxan, the treatment group 1 was induced with alloxan and Portulaca Oleracea leaf extract at a dose 60 mg/200grBW, treatment group 2 was induced with alloxan and Portulaca Oleracea leaf extract at a dose 90 mg/200grBW and treatment group 3 was induced by alloxan and Portulaca Oleracea leaf extract at a dose 110 mg/200grBW rats. Analysis of the results used the One Way Anova test followed by Post Hoc LSD analysis to see differences between groups.Results: The results of One Way Anova test on Malondialdehyde levels showed that there was an effect after intervention of Portulaca Oleracea leaf extract among the five treatment groups p = 0.000. The results of Post Hoc LSD test showed that Portulaca Oleracea leaf extract had effective inhibits the formation of malondialdehyde activity at a dose of 90 mg/200grBB p = 0.145.Conclusion: It can be concluded that Portulaca Oleracea leaf extract can reduce Malondialdehyde levels.&#x0D; &#x0D;

Chemical characterisation of sulfated polysaccharides from the red seaweed Centroceras clavulatum and their in vitro immunostimulatory and antioxidant properties

Phycocolloids have aroused research interest due to their remarkable functional properties, including immunostimulatory and antioxidant activities. In this study, the yield of Centroceras clavulatum sulfated polysaccharides (CCSP) was 4.36% and had a sulfate content of 9.42%. The main monosaccharide units of CCSP were galactose (25.23 ± 0.81 mg/l) and glucose (4.32 ± 0.31 mg/l). Specifically, FT-IR spectrum of CCSP revealed a peak at 843 cm−1 which indicates the occurrence of sulfate groups on C-4 of galactose. CCSP stimulated Carp Leukocyte Culture (CLC) cell line to generate reactive oxygen species (ROS) and nitric oxide (NO) in a dose-dependent manner. Remarkably, exposure of CLC cells to CCSP at a dose of 12.5 µg/ml significantly increased superoxide dismutase activity and reduced malondialdehyde level. These results suggest that CCSP could stimulate CLC cells without compromising the intracellular antioxidant system, hence, may have potential applications as nutraceuticals.

The Effect of Dendrophthoe pentandra (L.) Miq Ethanol Extract on Malondialdehyde (MDA) in Hyperglycemic Rats

Dendrophthoe pentandra (L.) Miq is a parasitic plant with medicinal potential found in 3000 other plant species. The duku parasite is usually considered a parasite on the duku plant and is often discarded because it is thought to interfere with the growth of the duku plant. The purpose of this study was to see the effect of the duku parasite leaf extract on the reduction of malondialdehyde (MDA) in hyperglycemic rats. MDA levels were measured by thiobarbituric acid-reactive substance (TBARS) assay with doses of duku mistletoe leaf ethanol extract of 400, 200, and 100 mg/kg BW. MDA levels were analysed using rat blood plasma, which was measured using a spectrophotometer at a wavelength of 532 nm. Oral administration of EEDBD 400, 200, and 100 mg/kg BW reduced MDA levels in hyperglycemic rats. However, only EEDBD 400 mg/kg BW showed a significant difference between the negative control (CMC-Na), but with glibenclamide and the normal groups, there was no significant difference.&#x0D;

Formulation Containing Phytosomes of Carotenoids from Nyctanthes arbor-tristis and Tagetes patula Protect D-galactose Induced Skin Aging in Mice

• Gel containing phytosomes of crocin rich extract(equivalent to crocin 1% w/w) obtained from Nyctanthes arbor-tristis and Lutein rich extract (equivalent to lutein 0.5%w/w) from Tagetes patula indicated • Entrapment of crocin and lutein was found to be (60.20% w/w) and (50.81% w/w) respectively. • Improved stability of crocin and lutein through preparation of Phytosomes • Significant (P<0.01) increase in thickness of dermal and epidermal layer • Significant increase (P<0.05) in glutathione level and decrease (P<0.01) in MDA level • Upregulation of expression of elastin and Collagen gene by 0.26 and 0.03 fold respectively : Carotenoids play important role in delay of aging process. Orange coloured tubular calyx of flowers of Nyctanthes arbor-tristis. contains crocin, an apocarotenoid which forms a major component of stigma of saffron. Due to presence of crocin in orange coloured tubular calyx of Nyctanthes arbor-tristis, it can be used as an economical substitute to saffron for its medicinal and cosmetic utilities. Lutein from flower petals of Tagetes patula L , is another popular carotenoid which has antioxidant effect and many health benefits. The carotenoids are highly unstable when exposed to atmosphere, hence in the present study crocin and lutein rich extracts were entrapped into phytosomes to improve stability and efficacy of topical preparation. : Oxidative stress is considered to be a major contributor to the process of aging. Carotenoids viz, Lutein and crocin, being powerful antioxidants, can delay aging of skin through upregulating col type I gene and elastin gene. The carotenoids have very low oxidation potential, due to which they get oxidized fast and protect oxidation of other compounds which make them highly unstable. One of the ways to improve stability of these phytoconstituents, is their entrapment in phytosomes. Preparation of phytosomes will have dual advantages of improving stability as well as bioavailability of molecule. : The phytosomes of Carotenoid rich extract of tubular calyx of Nyctanthes arbor-tristis L. and the petals of Tagetes patula L. (standardized for crocin and lutein content) were prepared using lipid film hydration technique and these phytosomes were then incorporated into gel base. The gel formulation was evaluated for stability as per ICH guidelines. Efficacy of formulation was evaluated by D-galactose induced aging model. Aging in skin was induced by administration of D-Galactose (100mg/kg b.w.s.c.) to albino mice for 42 days. The gel formulation was applied topically for 42 days. Then the effect of formulation on skin aging was evaluated by estimation of biochemical parameters viz. glutathione and malondialdehyde (MDA) and histopathological studies of treated skin samples. Also expression of COL type I and elastin genes was carried out from the skin samples by RT-PCR method. : Percent entrapment (%w/w) of crocin and lutein in phytosomes were found to be 60.20 and 50.81 respectively. Accelerated stability studies showed improvement in stability of carotenoids viz. crocin and lutein and the content of crocin and lutein in formulation was found in the range of 99.98 % w/w to 99.85%w/w at the end of three months. The formulation containing extract of Phytosomes of carotenoid rich extracts of Nyctanthes arbor-tristis L. and the petals of Tagetes patula L. exhibited potent antiaging activity through significant (p<0.05)increase in dermal and epidermal layers, and increase in GSH levels of skin as compared to the untreated group. The treatment with the gel formulation revealed upregulation of col type I and elastin genes. There was significant reduction in lipid peroxidation as revealed through reduction in MDA levels as compared to untreated group. : Crocin and lutein have potential to prevent skin aging via upregulation of COL type I gene and elastin gene. Upregulation of genes resulted into increase in the thickness of epidermal and dermal layer along with reduction in oxidative stress in skin. Entrapment of carotenoid rich extracts of Nyctanthes arbor-tristis and Tagetes patula in Phytosomes enhanced the stability and efficacy of the formulation.

Suppressive effect of black tea polyphenol theaflavins in a mouse model of ovalbumin-induced food allergy.

Food allergy is recognized as a global medical problem with increasing prevalence in recent years. Currently, the treatment of food allergy mainly involves avoidance of allergens and allergen-specific immunotherapy. Barring the spontaneous resolution of food allergy during the growth process, this disease is difficult to treat fundamentally. In recent years, the use of functional food ingredients derived from natural products has been attracting attention for their prophylactic use in food allergy. Theaflavins, i.e., black tea polyphenols, are potent antioxidants that have inhibitory effects on a variety of diseases. However, little is known about the preventive effect of theaflavins on food allergy. In this study, we designed a mouse model of food allergy and examined the effect of theaflavins using the severity of diarrhea, a symptom of food allergy, as an indicator. The administration of a black tea extract rich in theaflavins or theaflavin 1 (subgroup of theaflavins) to mice reduced the severity of diarrhea when compared with a normal diet. A reduction in malondialdehyde levels, a key marker of lipid peroxidation, was also observed. Overall, these data suggest that theaflavins may potentially inhibit food allergy by alleviating oxidative stress in the colon and can be a potential food material for prevention of food allergy.

Neuroprotective effects of alpha-lipoic acid on radiation-induced brainstem injury in rats.

Alpha-lipoic acid (ALA) is an antioxidant with radioprotective properties. We designed the current work to assess the neuroprotective function of ALA in the presence of oxidative stress induced by radiation in the brainstem of rats. Whole-brain radiations (X-rays) was given at a single dose of 25 Gy with or without pretreatment with ALA (200 mg/kg BW). Eighty rats were categorized into four groups: vehicle control (VC), ALA, radiation-only (RAD), and radiation + ALA (RAL). The rats were given ALA intraperitoneally 1 h before radiation and killed following 6 h, thereafter superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and total antioxidant capacity (TAC) in the brainstem were measured. Furthermore, a pathological examination was carried out after 24 h, 72 h, and five days to determine tissue damage. The findings indicated that MDA levels in the brainstem were 46.29 ± 1.64 μM in the RAD group and decreased in the VC group (31.66 ± 1.72 μM). ALA pretreatment reduced MDA levels while simultaneously increasing SOD and CAT activity and TAC levels (60.26 ± 5.47 U/mL, 71.73 ± 2.88 U/mL, and 227.31 ± 9.40 mol/L, respectively). The greatest pathological changes in the rat's brainstems were seen in RAD animals compared to the VC group after 24 h, 72 h, and 5 days. As a result, karyorrhexis, pyknosis, vacuolization, and Rosenthal fibers vanished in the RAL group in three periods. ALA exhibited substantial neuroprotectivity following radiation-induced brainstem damage.

Hesperidin Mitigates Cyclophosphamide-Induced Testicular Dysfunction via Altering the Hypothalamic Pituitary Gonadal Axis and Testicular Steroidogenesis, Inflammation, and Apoptosis in Male Rats.

Cyclophosphamide (CP) is a cytotoxic, cell cycle, non-specific, and antiproliferative drug. This study aimed to address the toxic effects of CP on male fertility and the possible ameliorative role of hesperidin (HSP). Thirty-two adult albino rats were randomly divided into four groups, namely, the negative control, HSP, CP-treated, and CP+HSP-treated groups. The CP-treated rats showed a significant reduction in the levels of serum LH, FSH, testosterone, prolactin, testicular glutathione peroxidase (GPx), and total antioxidant capacity (TAC) with an elevation in levels of malondialdehyde (MDA), and p53, and iNOS immune expression, compared to the control group. A significant downregulation in hypothalamic KISS-1, KISS-1r, and GnRH, hypophyseal GnRHr, and testicular mRNA expression of steroidogenesis enzymes, PGC-1α, PPAR-1, IL10, and GLP-1, as well as a significant upregulation in testicular mRNA of P53 and IL1β mRNA expression, were detected in the CP-treated group in comparison to that in the control group. The administration of HSP in CP-treated rats significantly improved the levels of serum LH, FSH, testosterone, prolactin, testicular GPx, and TAC, with a reduction in levels of MDA, and p53, and iNOS immune expression compared to the CP-treated group. A significant upregulation in hypophyseal GnRHr, and testicular mRNA expression of CYP19A1 enzymes, PPAR-1, IL10, and GLP-1, as well as a significant downregulation in testicular mRNA of P53 and IL1β mRNA expression, were detected in the CP+HSP-treated group in comparison to that in the CP-treated group. In conclusion, HSP could be a potential auxiliary agent for protection from the development of male infertility.

Functional Characterization of Lobularia maritima LmTrxh2 Gene Involved in Cold Tolerance in Tobacco through Alleviation of ROS Damage to the Plasma Membrane.

Cold stress is a key environmental factor affecting plant growth and development, crop productivity, and geographic distribution. Thioredoxins (Trxs) are small proteins that are ubiquitously expressed in all organisms and implicated in several cellular processes, including redox reactions. However, their role in the regulation of cold stress in the halophyte plant Lobularia maritima remains unknown. We recently showed that overexpression of LmTrxh2, which is the gene that encodes the h-type Trx protein previously isolated from L. maritima, led to an enhanced tolerance to salt and osmotic stress in transgenic tobacco. This study functionally characterized the LmTrxh2 gene via its overexpression in tobacco and explored its cold tolerance mechanisms. Results of the RT-qPCR and western blot analyses indicated differential temporal and spatial regulation of LmTrxh2 in L. maritima under cold stress at 4 °C. LmTrxh2 overexpression enhanced the cold tolerance of transgenic tobacco, as evidenced by increased germination rate, fresh weight and catalase (CAT), superoxide dismutase (SOD) and peroxidase (POD) activities; reduced malondialdehyde levels, membrane leakage, superoxide anion (O2-), and hydrogen peroxide (H2O2) levels; and higher retention of chlorophyll than in non-transgenic plants (NT). Furthermore, the transcript levels of reactive oxygen species (ROS)-related genes (NtSOD and NtCAT1), stress-responsive late embryogenis abundant protein 5 (NtLEA5), early response to dehydration 10C (NtERD10C), DRE-binding proteins 1A (NtDREB1A), and cold-responsive (COR) genes (NtCOR15A, NtCOR47, and NtKIN1) were upregulated in transgenic lines compared with those in NT plants under cold stress, indicating that LmTrxh2 conferred cold stress tolerance by enhancing the ROS scavenging ability of plants, thus enabling them to maintain membrane integrity. These results suggest that LmTrxh2 promotes cold tolerance in tobacco and provide new insight into the improvement of cold-stress resistance to cold stress in non-halophyte plants and crops.

S-adenosylmethionine improves cognitive impairment in D-galactose-induced brain aging by inhibiting oxidative stress and neuroinflammation

Oxidative stress and neuroinflammation play crucial roles in aging. S-adenosylmethionine (SAM), a popular supplement, is a potential antioxidant and candidate therapy for depression. This study aimed to evaluate the neuroprotective effects of SAM on D-galactose-induced brain aging and explore its underlying mechanisms. Brain aging model was established with D-galactose (180 mg/kg/day) for 8 weeks. During the last 4 weeks, SAM (16 mg/kg) was co-administrated with D-galactose. Behavior tests were used to assess cognitive function and depression-like behaviors of rats. Results showed that cognitive impairment and depression-like behaviors were reversed by SAM. SAM reduced neuronal cell loss, increased brain-derived neurotrophic factor level in the hippocampus, inhibited amyloid-β level and microglia activation, as well as pro-inflammatory factors levels in the hippocampus and serum. Further, SAM enhanced antioxidant capacity and attenuated cholinergic damage by reducing malondialdehyde levels, increasing acetylcholine levels, expression levels of α7 nicotinic acetylcholine receptor (α7nAChR), nuclear factor erythrocyte 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in the hippocampus. Above all, SAM has a potential neuroprotective effect on ameliorating cognitive impairment in brain aging, which is related to inhibition of oxidative stress and neuroinflammation, as well as α7nAChR signals. Data AvailabilityData will be made available on request.

The Combined Effect of Licorice Extract and Bone Marrow Mesenchymal Stem Cells on Cisplatin-Induced Hepatocellular Damage in Rats.

Drug-induced liver damage is a life-threatening disorder, and one major form of it is the hepatotoxicity induced by the drug cisplatin. In folk medicine, Licorice (Glycyrrhiza glabra (is used for detoxification and is believed to be a potent antioxidant. Currently, the magically self-renewable potential of bone marrow mesenchymal stem cells (BM-MSCs) has prompted us to explore their hepatoregenerative capability. The impact of G. glabra extract (GGE) and BM-MSCs alone and, in combination, on protecting against hepatotoxicity was tested on cisplatin-induced liver injury in rats. Hepatic damage, as revealed by liver histopathology and increased levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and malondialdehyde (MDA), was elevated in rats by received 7 mg/kg of cisplatin intraperitoneally. The combination of GGE and BM-MSCs returned the enzyme levels to near the normal range. It also improved levels of liver superoxide dismutase (SOD) and glutathione (GSH) and reduced MDA levels. Additionally, it was found that when GGE and BM-MSCs were used together, they significantly downregulated caspase9 (Casp9), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), and interleukin-1β (IL-1β), which are involved in severe proinflammatory and apoptotic signaling cascades in the liver. Moreover, combining GGE and BM-MSCs led to the normal result of hepatocytes in several examined liver histological sections. Therefore, our findings suggest that GGE may have protective effects against oxidative liver damage and the promising regenerative potential of BM-MSCs.

Antioxidant Mechanisms Underlying the Gastroprotective Effect of Menthofuran on Experimentally Induced Gastric Lesions in Rodents.

Menthofuran is a monoterpene present in various essential oils derived from species from Mentha genus, and in Brazil, those species are widely used in treating gastrointestinal and respiratory disorders. Considering the wide pharmacological potential of monoterpenes, including their antioxidant activity, this study aimed to evaluate menthofuran-gastroprotective activity, as well as the involvement of antioxidant mechanisms in this effect. The acute toxicity was evaluated according to the fixed dose method. The antiulcerogenic activity was investigated by using experimental models of gastric ulcers induced by ethanol, indomethacin, and ischemia/reperfusion in rats. The antisecretory gastric activity, the catalase activity, and the gastric wall mucus were determined in pylorus ligated rats. Gastric wall nonprotein sulfhydryl (NPSH) group content, myeloperoxidase (MPO) activity, and malondialdehyde (MDA) content were evaluated in ethanol-induced the gastric ulcer model. Menthofuran (2 g/kg) presented low acute toxicity and showed gastroprotective activity against ethanol-, indomethacin-, and ischemia/reperfusion-induced ulcers. Moreover, menthofuran presented antisecretory activity, reduced the total acidity, and increased pH of gastric secretion. On the other hand, a decrease in mucus content of gastric wall without alteration of gastric juice volume and catalase activity was observed. Interestingly, menthofuran increased NPSH levels and reduced MDA levels and MPO activity. Gastroprotective effects of menthofuran appear to be mediated, at least in part, by the NOS pathway, endogenous prostaglandins, reduced gastric juice acidity, increased concentration of the NPSH groups, and reduced lipidic peroxidation. These findings support the menthofuran as an effective gastroprotective agent, as well as the marked participation of antioxidant mechanisms in this response.

Sericin improves memory and sociability impairments evoked by transient global cerebral ischemia through suppression of hippocampal oxidative stress, inflammation, and apoptosis.

Sericin (Ser) is a natural neuroactive macromolecule with diverse pharmacological properties, and our previous findings have shown its neuroprotective potentials. This study aimed to investigate the therapeutic potential of Ser on cognitive dysfunction induced by transient global cerebral ischemia/reperfusion (tGI/R) and its mechanism of action. The tGI/R was induced in BALB/c mice by bilateral occlusion of the common carotid arteries for two 5 min followed by a 10-min reperfusion period. After 24 h, mice were treated with normal saline or different doses of Ser (100, 200, and 300 mg/kg) for 10 days. Cognitive performances were assessed using the Barnes maze and social interaction tasks. Oxidative stress markers including superoxide dismutase (SOD), glutathione peroxidase (GPx), total antioxidant capacity (TAC), and malondialdehyde (MDA) as well as pro-inflammatory cytokines (interleukin (IL)-6 and tumor necrosis factor-alpha) and anti-inflammatory cytokine (IL-10) were assessed in the hippocampus. Markers of apoptosis (pro- and cleaved caspase-9 and 3, Bax, and Bcl-2) were assessed by Western blotting. Besides, transferase-mediated dUTP nick end-labeling assay was used to detect apoptotic cell death. We show here that Ser administration improved tGI/R-induced cognitive deficits, enhanced the activity of SOD and GPx, increased TAC levels, while reduced MDA levels. Notably, Ser decreased neuronal apoptotic cell death in the hippocampal dentate gyrus (DG) region, accompanied by suppression of neuroinflammation, downregulation of pro-apoptotic proteins (caspase-9, caspases-3, and Bax), and upregulation of anti-apoptotic protein, Bcl-2. Taken together, Ser administration protected hippocampal neurons from apoptotic cell death by impeding oxidative stress and inflammatory responses and, in turn, improved cognitive function in the tGI/R mice.