Effects Of Resveratrol Research Articles

Resveratrol Mitigates Ischemia/Reperfusion-Induced Cardiomyocyte Injury by Inhibiting the Expression of Superoxide Dismutase 2

Resveratrol exhibits antioxidant, anti-inflammatory, and potentially cardio-protective properties. However, the effectiveness of resveratrol in acute myocardial infarction (AMI)-induced cardiomyocyte injury remains unclear. Superoxide Dismutase 2 (SOD2) is an important antioxidant enzyme in the mitochondria. However, few studies have reported the impact of SOD2 on AMI-induced cardiomyocyte injury. Therefore, we establish an in vitro model of cardiomyocyte ischemia/reperfusion (I/R) injury using oxygen-glucose deprivation/reoxygenation (OGD/R) to investigate the protective effects of resveratrol against OGD/R-induced cardiomyocyte injury and its underlying regulatory mechanism. Cell viability was assessed using the CCK-8. Apoptosis was evaluated by TUNEL staining. The levels of Cleaved cas-3, Bcl2, and SOD2 an important antioxidant enzyme in the mitochondria that is responsible for eliminating superoxide radicals were analyzed by western blot. The ROS positive rate was using a ROS/Superoxide detection assay kit. The relative abundance of the SOD2 mRNA was determined using the 2−ΔΔCT method. We demonstrated that OGD/R treatment significantly reduced AC16 cell viability while increasing apoptosis levels, oxidative stress, and inflammatory factor levels. We further confirmed the upregulation of SOD2 by OGD/R treatment, suggesting its potential involvement in modulating OGD/R-induced AC16 cell injury. Additionally, silencing SOD2 ameliorated the detrimental effects of OGD/R on AC16 cells. Moreover, we observed that upregulation of SOD2 aggravated OGD/R-induced AC16 cell injury, and resveratrol effectively reduced OGD/R-induced AC16 cell injury by down-regulating SOD2. In conclusion, this research provides a promising therapeutic strategy for mitigating I/R damage in AMI-induced cardiomyocytes, thereby identifying a potential target for therapeutic intervention.

Investigating the Effect of Resveratrol on The Survival Rate of 4T1 Breast Cancer Cells By MTT Method

Cancer is known as an incurable, deadly and deadly disease with pain and disability. During recent decades, changes in people's lifestyles have increased the incidence and prevalence of breast cancer worldwide. With the wide spread of this disease, research has also increased on this issue. Resveratrol is known as a natural polyphenol found in red grapes and some other foods, and with its important anti-cancer properties, it can be effective in reducing the risk of breast cancer and its treatment. Research has shown that resveratrol can have positive effects on breast cancer by reducing DNA methylation, reducing cell proliferation, and reducing cancer growth factors. In this research, resveratrol has been used against 4T1 cancer cells, which were treated with different concentrations of resveratrol after cultivation in 96-well plates and measured by the MTT method. The obtained results showed that resveratrol in all concentrations and at different times significantly reduces the survival of 4T1 cancer cells. By increasing the concentration and treatment time, the decrease in cell viability increases. This indicates strong, dose- and time-dependent effects of resveratrol on breast cancer cells.

The antioxidant protective effect of resveratrol on long-term exposure to acrylamide-induced skeletal toxicity in female mice.

Acrylamide (AA) is a toxic substance formed when cooking starch-based foods at high temperatures. Studies have shown that AA can cause neurotoxicity, reproductive toxicity and so on. However, there remains limited understanding of the potential skeletal toxicity of AA. The aim of this study was to investigate the potential skeletal toxicity of AA, as well as the potential bone protective effects of Resveratrol (RVT). Based on the daily intake of adult women, adult female mice was treated with AA at 0, 0.01, 0.1, 1 mg/kg/d or AA/RVT (1 mg/kg/d AA +10 mg/kg/d RVT) for 8 weeks, and skeletal toxicity were evaluated by RT-qPCR and histopathological techniques. The results found that exposure to AA (0.1 or 1 mg/kg/d) after 8 weeks, osteogenesis exhibited pathological damage characteristics such as inhibition of growth plate function, and reduction of fibrous tissue, and cartilage exhibited pathological damage characteristics such as irregular cell morphology and arrangement, and damage to the tidal line. The results of cellular functional gene testing showed a decrease in the expression of functional genes in osteoblasts and chondrocytes. Meanwhile, after further co-treatment with AA (1 mg/kg/d) and resveratrol (RVT) (10 mg/kg/d), we found that RVT restored AA-induced damage to osteogenesis and cartilage, and reduced the high apoptosis and oxidative stress levels in osteogenesis/cartilage after AA exposure. In summary, this study confirmed the skeletal toxicity of AA on female adult mice, and further clarified the antioxidant protective effect of RVT on this toxicity.

Ameliorative effect of resveratrol against type 2 diabetes in rats through triggering of autophagy and inhibition of mTOR pathway.

Ameliorative effect of resveratrol against type 2 diabetes in rats through triggering of autophagy and inhibition of mTOR pathway.

Protective Role of Resveratrol Against Toluene-Induced Oxidative Stress in Rats

Toluene is a toxic substance commonly used in the industry that leads to oxidative stress in the body and causes in the formation of reactive oxygen species. In addition to the antioxidants produced by our body, we also obtain antioxidants through foods. Resveratrol is a polyphenol found in many plant species and possesses antioxidant properties. The effects of oxidative stress induced by toluene and the protective effect of resveratrol were investigated through changes in malondialdehyde (MDA) and glutathione (GSH) levels. Male rats were administered different doses of toluene and resveratrol (5 mg/kg, 10 mg/kg, 20 mg/kg), while control groups were given physiological saline and ethanol. At the end of the experiment, blood and lung tissues of the animals were examined, and MDA and GSH levels were measured. According to the obtained data, a significant increase in GSH activity was observed after the administration of toluene. However, in groups treated with combinations of toluene and various doses of resveratrol, a significant decrease in GSH levels was detected. While a significant increase in MDA levels in lung tissues was observed between the control groups and the toluene group, no significant change was observed in blood samples.

Resveratrol shields against cisplatin-induced ototoxicity through epigenetic lncRNA GAS5 modulation of miR-455-5p/PTEN pathway

BackgroundOur previous research demonstrated that resveratrol counters DDP-induced ototoxicity by upregulating miR-455-5p, which targets PTEN. This study aimed to elucidate the underlying mechanisms involving GAS5 and DNA methyltransferase 1 (DNMT1) in resveratrol’s protective action. MethodsA luciferase reporter assay and RNA immunoprecipitation (RIP) assay were employed to study the binding between GAS5 and miR-455-5p, as well as between miR-455-5p and PTEN. HEI-OC1 cells treated with DDP were transfected with vectors for GAS5, si-GAS5, DNMT1, si-DNMT1, and miR-455-5p mimics, as well as PTEN. Subsequently, they were treated with resveratrol and exposed to DDP, both separately and in combination. The distribution of CpG islands in the GAS5 promoter was identified using MethyPrimer, and methylation-specific PCR (MSP) was conducted to determine the methylation levels of GAS5. Chromatin immunoprecipitation (ChIP) was utilized to examine the interaction between DNMT1 and GAS5. The viability of HEI-OC1 cells, catalase (CAT) activity, apoptosis, and ROS levels were assessed using the CCK-8 assay, CAT assay, TUNEL staining, and flow cytometry, respectively. An in vivo mouse model was developed to measure auditory brainstem response (ABR) thresholds, while RT-qPCR and Western blot analysis were employed to evaluate molecular levels. ResultsOur study discovered that GAS5 acts as a sponge for miR-455-5p, thereby increasing PTEN expression in DDP-treated HEI-OC1 cells. This process was reversed upon treatment with resveratrol. Importantly, DNMT1 promoted the methylation of the GAS5 promoter, leading to the suppression of GAS5 expression. This suppression enhanced the effectiveness of resveratrol in combating DDP-induced apoptosis and ROS in HEI-OC1 cells and amplified its protective effect against DDP’s ototoxicity in vivo. ConclusionsOur research emphasizes the significance of the DNMT1/GAS5/miR-455-5p/PTEN axis as a promising new route to boost resveratrol’s effectiveness against DDP-induced ototoxicity.

A Study on the Protective Impact of Resveratrol on Liver Damage in Rats with Obstructive Jaundice.

Obstructive Jaundice (OJ) is a common clinical condition with potential outcomes, including hepatocyte necrosis, bile duct hyperplasia, significant cholestatic liver fibrosis, and, in severe cases, liver failure. Resveratrol (RES), a polyphenol present in grapes and berries, has demonstrated efficacy in improving OJ. However, the precise mechanism of its action remains unclear. In this study, we employed network pharmacology to investigate the underlying molecular mechanism of RES in the treatment of OJ. The targets of RES were identified using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), SuperPred, and SwissTargetPrediction database. The targets related to OJ were gathered from the DisGeNET, GeneCards, DrugBank, and Online Mendelian Inheritance in Man (OMIM) databases, and the intersection of these targets was determined using Venny2.1.0. Subsequently, an active component-target network was constructed using Cytoscape software. The Protein-Protein Interaction (PPI) network was generated using the String database and Cytoscape software. Following this, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted using the Bioconductor platform. Finally, quantitative Real-Time PCR (qRT-PCR), Western Blotting (WB), and Enzyme-Linked Immunosorbent Assay (ELISA) were employed to assess RNA and protein expression levels in related pathways. The findings revealed a selection of 56 potential targets for RES, and a search through the online database identified 2,742 OJ-related targets with overlapping in 27 targets. In the PPI network, mTOR, CYP2C9, CYP1A1, CYP3A4, AHR, ESR1, and HSD17B1 emerged as core targets. KEGG analyses demonstrated that the primary pathways of RES in treating OJ, particularly those related to lipid metabolism, include linoleic acid metabolism, arachidonic acid metabolism, metabolism of xenobiotics by cytochrome P450, lipid and atherosclerosis, tyrosine metabolism, steroid hormone biosynthesis, and pentose and glucuronate interconversions signaling pathways. Furthermore, in vivo experiments indicated that RES significantly ameliorated liver injury induced by Common Bile Duct Ligation (CBDL) in rats with OJ. It lowered serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, reduced liver tissue MDA levels, increased glutathione (GSH) content, and enhanced activity of superoxide dismutase (SOD), alleviating liver damage. Metabolomics analysis revealed that the therapeutic effect of RES in OJ involved alterations in lipid metabolic pathways, hinting at the potential mechanism of RES in treating OJ. ELISA, qRTPCR, and WB analyses confirmed lower expression levels of mTOR, CYP1A1, and CYP2C9 in the RES group compared to the model group, validating their involvement in the lipid metabolism pathway. In conclusion, RES exhibited a protective effect on liver function in rats with OJ. The underlying mechanism appears to be linked to antioxidant activity and modulation of lipid metabolism pathways.

Resveratrol Induces Myotube Development by Altering Circadian Metabolism via the SIRT1-AMPK-PP2A Axis.

Resveratrol is a polyphenol known to have metabolic as well as circadian effects. However, there is little information regarding the metabolic and circadian effect of resveratrol on muscle cells. We sought to investigate the metabolic impact of resveratrol throughout the circadian cycle to clarify the associated signaling pathways. C2C12 myotubes were incubated with resveratrol in the presence of increasing concentrations of glucose, and metabolic and clock proteins were measured for 24 h. Resveratrol led to SIRT1, AMPK and PP2A activation. Myotubes treated with increasing glucose concentrations showed higher activation of the mTOR signaling pathway. However, resveratrol did not activate the mTOR signaling pathway, except for P70S6K and S6. In accordance with the reduced mTOR activity, resveratrol led to advanced circadian rhythms and reduced levels of pBMAL1 and CRY1. Resveratrol increased myogenin expression and advanced its rhythms. In conclusion, resveratrol activates the SIRT1-AMPK-PP2A axis, advances circadian rhythms and induces muscle development.

Effects of resveratrol on changes in trimethylamine-N-oxide and circulating cardiovascular factors following exercise training among older adults

PurposeTrimethylamine-N-oxide (TMAO) is a gut-derived metabolite associated with cardiovascular disease (CVD). In preclinical and observational studies, resveratrol and exercise training have been suggested as potential strategies to reduce the systemic levels of TMAO. However, evidence from experimental studies in humans remains unknown. This project examined the dose-dependent effects of a combined resveratrol intervention with exercise training on circulating TMAO and other related metabolite signatures in older adults with high CVD risk. MethodsForty-one older adults [mean (±SD) age of 72.1 (6.8) years] participated in a 12-week supervised center-based, multi-component exercise training intervention [2×/week; 80 min/session] and were randomized to one of two resveratrol dosages [Low: 500 vs. High:1000 mg/day] or a cellulose-based placebo. Serum/plasma were collected at baseline and post-intervention and evaluated for TMAO and associated analytes. ResultsAfter the 12-week intervention, TMAO concentration increased over time, regardless of treatment [mean (±SD) Placebo: 11262 (±3970); Low:13252 (±1193); High: 12661(±3359) AUC; p = 0.04]. Each resveratrol dose produced different changes in metabolite signatures. Low dose resveratrol upregulated metabolites associated with bile acids biosynthesis (i.e., glycochenodeoxycholic acid, glycoursodeoxycholic acid, and glycocholic acid). High dose resveratrol modulated metabolites enriched for glycolysis, and pyruvate, propanoate, β-alanine, and tryptophan metabolism. Different communities tightly correlated to TMAO and resveratrol metabolites were associated with the lipid and vascular inflammatory clinical markers [|r| > 0.4, p < 0.05]. ConclusionThese findings suggest a distinct dose-dependent adaptation response to resveratrol supplementation on circulating metabolite signatures but not on TMAO among high-risk CVD older adults when combined with an exercise training intervention.

The Effects of Dietary Resveratrol and β-Hydroxy-β-Methylbutyric Acid Supplementation at Two Protein Levels on the Ruminal Microbiome and Metabolome of Tibetan Sheep

Resveratrol (RES) and β-hydroxy-β-methylbutyric acid (HMB) have antioxidant, anti-inflammatory, and other beneficial properties. Here, we hypothesize that supplementation with RES and HMB could affect the rumen function in Tibetan sheep. This study aims to explore the effects of RES and HMB supplementation at different protein levels on the rumen microbial and metabolite compositions of Tibetan sheep. Four treatments (n = 30) were prepared according to a 2 × 2 factorial arrangement, with two dietary protein levels (12% and 14%) and two feed additives (RES 1.50 g/day and HMB 1.25 g/day). The experimental treatments were fed diets with 12% CP level non-supplemented (L), 12% protein with RES and HMB (L-RES-HMB), 14% CP level non-supplemented (H), and 14% protein with RES and HMB (H-RES-HMB), respectively. Our results indicated that the trypsin, chymotrypsin, and lipase were significantly increased in the H-RES-HMB group (p &lt; 0.05), while the lipopolysaccharide (LPS) concentration was significantly reduced (p &lt; 0.05). The alpha diversity analysis found that the ACE indices of the L-RES-HMB, and H-RES-HMB groups was significantly higher than that of the L group (p &lt; 0.05). Additionally, compared with the L, L-RES-HMB, and H groups, it was found that the abundance of Euryarchaeota, Spirochaeota, and Metanobrevibacter was significantly increased in the H-RES-HMB group, while the abundance of Proteobacteria was significantly decreased (p &lt; 0.05). A total of 745 significantly different metabolites were identified, of which 14 metabolites were common among the three comparative groups. Differential metabolites were mainly enriched in pathways including the pyrimidine metabolism, the glycine, serine, and threonine metabolisms, and ABC transporters. Overall, CP level and RES/HMB exhibited positively interaction effect on digestive enzyme activity and antioxidant capacity. Dietary RES and HMB supplementation on 14% CP level improved the ruminal digestive enzyme activity and antioxidant capacity through modulating the microbial community and regulating the metabolism.

Resveratrol activates MAPK/ERK pathway to regulate oestrogen metabolism in type I endometrial cancer

ObjectiveEndometrial cancer (EC) is an oestrogen-dependent tumour, the occurrence of which is closely related to an imbalance of oestrogen homeostasis. Our previous studies explored the effects of Resveratrol(Res) on oestrogen metabolism. However, systematic research on the exact mechanism of action of Res is still lacking. Based on network pharmacology, molecular docking and animal experiments, the effects and molecular mechanisms of Res on endometrial cancer were investigated.MethodsThe target of Res was obtained from the high-throughput experiment and reference-guided database of TCM (HERB) and the Encyclopedia of Traditional Chinese Medicine (ETCM) databases, and the target of endometrial cancer was obtained by using the Genecards database. Venny map was used to obtain the intersection target of Res in the treatment of endometrial cancer, and the protein interaction network of the intersection target was constructed by importing the data into the STRING database. Then, the drug–disease–target interaction network was constructed based on Cytoscape 3.9.1 software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed for intersection targets using the OmicShare cloud platform. Res and core targets were analysed by molecular docking. EC model mice induced by MNNG were randomly divided into the control group, Res group, MNNG group, MNNG + Res group, and MNNG + Res + MAPK/ERKi group. The protein levels of ERK and p-ERK in the mouse uterus were detected by Western blot. The levels of E1, E2, E3, 16-epiE3, 17-epiE3, 2-MeOE1, 4-MeOE1, 2-MeOE2, 4-MeOE2, 3-MeOE1, 2-OHE1, 4-OHE1, 2-OHE2, 4-OHE2, and 16α-OHE1 in the serum and endometrial tissue of mice were measured by LC‒MS/MS.ResultsA total of 174 intersection targets of Res anti-endometrial cancer were obtained. The signalling pathways analysed by KEGG enrichment included the AGE-RAGE signalling pathway in diabetic complications, the PI3K-Akt signalling pathway and the MAPK signalling pathway. The top 10 core targets were MAPK3, JUN, TP53, CASP3, TNF, IL1B, AKT1, FOS, VEGFA and INS. Molecular docking showed that in addition to TNF, other targets had good affinity for Res, and the binding activity with MAPK3 was stable. Western blot results showed that Res increased the phosphorylation level of ERK and that MAPK/ERKi decreased ERK activation. In the LC-MS/MS analysis, the levels of 2-MeOE1, 2-MeOE2 and 4-MeOE1 in serum and uterine tissue showed a significantly decreasing trend in the MNNG group, while that of 4-OHE2 was increased (P < 0.05). The concentrations of 4-MeOE1 in serum and 2-MeOE1 and 2-MeOE2 in the endometrial tissue of mice were significantly increased after Res treatment, and those of 4-OHE2 in the serum and uterus of mice were significantly decreased (P < 0.05). Meanwhile, in the MAPK/ERKi intervention group, the effect of Res on the reversal of oestrogen homeostasis imbalance was obviously weakened.ConclusionRes has multiple targets and multiple approaches in the treatment of endometrial cancer. In this study, it was found that Res regulates oestrogen metabolism by activating the MAPK/ERK pathway. This finding provides a new perspective for subsequent research on the treatment of endometrial cancer.

Effects of zinc and resveratrol as modulators of leptin response in adults with obesity

fat tissue is an organ with endocrine function, where the hormone leptin (LEP) is identified. This peptide regulates appetite, the immune system, vascular functions and insulin sensitivity. Zinc (Zn) and resveratrol (RES) have potential effects on adipose tissue. to know if the combined administration of Zn and RES has any effect on blood leptin quantification in obese people. longitudinal experimental study, controlled clinical trial design, randomized, double blind. Randomized formation of four groups: T1 (Zn 50 mg), T2 (control), T3 (RES 500 mg), T4 (Zn 50 mg and RES 500 mg) with a supplementation period of 60 days. Blood samples were taken and glucose (GLU), leptin (LEP) and lipids (HDL, LDL, TGL) were quantified before and after exposure to the study elements. age 34 (± 7) years. In T-tests, significance in GLU (p = 0.04) and LEP (p = 0.055). By exposure groups: GLU at T1 (p = 0.03) and T2 (p = 0.031); at LEP at T4 (p = 0.024). Lipids by groups: HDL at T3 (p = 0.039) and T4 (p = 0.014). ANOVA, HDL (p = 0.06). Pearson, HDL (p = 0.07) and LDL (p = 0.09). zinc and resveratrol showed promise as agents in modulating leptin and glucose signaling, confirming that they work in a proportional manner and provide benefits for cardiac health, but more exposure time is needed to see if they impact energy balance homeostasis.

Multifaceted Impacts of Monosodium Glutamate on Testicular Health: Insights into Pyroptosis and Therapeutic Potential of Resveratrol.

Monosodium glutamate was considered one of the food additive and flavor enhancer in processed meat and soup that affects testicular tissues, the aim of this research to investigates the impact of monosodium glutamate (MSG) on testicular structure in rats and explores the potential protective effects of resveratrol. Four experimental groups involved in our study 10 rats of each.: the first group as control group; the second group (Resveratrol group: control rats received 20 mg/kg of resveratrol, via oral gavage); the third group (MSG group: rats received monosodium glutamate (MSG) with a dose 60 mg/kg body weight daily, via gastric tube, and the fourth group (MSG+ Resveratrol group). Serum level of testosterone, FSH, LH, were measured. Testicular tissues were prepared for measurement of oxidative stress markers, and gene expression of NLRP3, Caspase 3, and GSK-3β. Moreover, paraffin blocks contained testicular tissue used for histological and immunohistochemical examination. Additionally, seminal smear from epididymis were examined. MSG administration adversely affected testosterone production, hormonal levels, and sperm parameters, Histological examination revealed marked testicular degeneration, and oxidative stress assessments indicated elevated level of MDA a lipid peroxidation marker and decrease in SOD, CAT antioxidant enzymes. Moreover, MSG-induced apoptotic and pyroptotic markers and its gene expressions. Importantly. Administration of resveratrol reversed the detrimental effects of MSG, demonstrating its corrective influence on the hypothalamic-pituitary-gonadal axis disruption, improvement of sperm parameters, attenuation of oxidative stress, anti-apoptotic activity, and anti-pyroptotic effects. The expression of Ki-67 as a cell proliferation marker further supported the positive response to spermatogenesis dysfunction upon resveratrol treatment. This comprehensive exploration sheds light on the protective effect of resveratrol against MSG-induced testicular with exploration of its mechanistic role.

Protective effect and mechanism of resveratrol on vascular endothelial cells

Resveratrol is a polyphenolic plant extract with many biological activities such as anti-inflammation and anti-oxidative stress. Vascular endothelial cell (VEC) is the main sites for maintaining normal vascular permeability and participating in vasomotor regulation and substance exchange. VEC injury plays a key role in various diseases or pathological processes such as cardiovascular disease, chronic inflammation and sepsis. Studies have shown that resveratrol protects VEC and reduces endothelial damage by regulating nitric oxide (NO) and its related enzymes, reducing oxidative stress and inhibiting apoptosis, thereby exerting beneficial effects.

Resveratrol Inhibits VDAC1-Mediated Mitochondrial Dysfunction to Mitigate Pathological Progression in Parkinson's Disease Model.

An increase in α-synuclein (α-syn) levels and mutations in proteins associated with mitochondria contribute to the development of familial Parkinson's disease (PD); however, the involvement of α-syn and mitochondria in idiopathic PD remains incompletely understood. The voltage-dependent anion channel I (VDAC1) protein, which serves as a crucial regulator of mitochondrial function and a gatekeeper, plays a pivotal role in governing cellular destiny through the control of ion and respiratory metabolite flux. The ability of resveratrol (RES), which is a potent phytoalexin with antioxidant and anti-inflammatory properties, to regulate VDAC1 in PD is unknown. The objective of this study was to evaluate the role of VDAC1 in the pathological process of PD and to explore the mechanism by which resveratrol protects dopaminergic neurons by regulating VDAC1 to maintain the mitochondrial permeability transition pore (mPTP) and calcium ion balance. The effects of RES on the motor and cognitive abilities of A53T mice were evaluated by using small animal behavioral tests. Various techniques, including immunofluorescence staining, transmission electron microscopy, enzyme-linked immunoadsorption, quantitative polymerase chain reaction (PCR), and Western blotting, among others, were employed to assess the therapeutic impact of RES on neuropathy associated with PD and its potential in regulating mitochondrial VDAC1. The findings showed that RES significantly improved motor and cognitive dysfunction and restored mitochondrial function, thus reducing oxidative stress levels in A53T mice. A significant positive correlation was observed between the protein expression level of VDAC1 and mitochondrial α-syn expression, as well as disease progression, whereas no such correlation was found in VDAC2 and VDAC3. Administration of RES resulted in a significant decrease in the protein expression of VDAC1 and in the protein expression of α-syn both in vivo and in vitro. In addition, we found that RES prevents excessive opening of the mPTP in dopaminergic neurons. This may prevent the abnormal aggregation of α-syn in mitochondria and the release of mitochondrial apoptosis signals. Furthermore, the activation of VDAC1 reversed the resveratrol-induced decrease in the accumulation of α-syn in the mitochondria. These findings highlight the potential of VDAC1 as a therapeutic target for PD and identify the mechanism by which resveratrol alleviates PD-related pathology by modulating mitochondrial VDAC1.

Effect of Resveratrol and Curcumin on Changes in Fatty Acid Composition and Oxidative Stress in Liver and Kidney Tissues of Rats Exposed to 7,12-Dimethylbenz[a]anthracene (DMBA)

Effect of Resveratrol and Curcumin on Changes in Fatty Acid Composition and Oxidative Stress in Liver and Kidney Tissues of Rats Exposed to 7,12-Dimethylbenz[a]anthracene (DMBA)

Enhancing the Anti-Tumor Efficacy of NK Cells on Canine Mammary Tumors through Resveratrol Activation.

In order to explore the therapeutic effect of Resveratrol (Res)-activated Natural Killer (NK) cells on canine mammary tumors, this study employed a range of assays, including wound healing, colony formation, Transwell, flow cytometry, and Western blot experiments, to investigate the impact of Res-pretreated NK cells on canine mammary tumor cells in vitro. Additionally, a tumor-bearing mouse model was utilized to further analyze the therapeutic effects of Res-pretreated NK cells in vivo. The results showed that Res enhances the capacity of NK cells to induce apoptosis, pyroptosis, and ferroptosis in canine breast tumor cells, while also augmenting their influence on the migration, invasion, and epithelial-mesenchymal transition of these cells. Furthermore, pretreatment of NK cells with Res significantly amplified their inhibitory effect on breast tumor growth in vivo and promoted tumor tissue apoptosis. Additionally, Res enhanced the recruitment of NK cells to other immune cells in the body. In summary, Res has been shown to enhance the anti-breast-tumor effect of NK cells both in vitro and in vivo, offering a new avenue for optimizing immunotherapy for canine breast tumors.

Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma in rodents: A narrative review.

Glaucoma, an irreversible optic neuropathy, primarily affects retinal ganglion cells (RGC) and causes vision loss and blindness. The damage to RGCs in glaucoma occurs by various mechanisms, including elevated intraocular pressure, oxidative stress, inflammation, and other neurodegenerative processes. As the disease progresses, the loss of RGCs leads to vision loss. Therefore, protecting RGCs from damage and promoting their survival are important goals in managing glaucoma. In this regard, resveratrol (RES), a polyphenolic phytoalexin, exerts antioxidant effects and slows down the evolution and progression of glaucoma. The present review shows that RES plays a protective role in RGCs in cases of ischemic injury and hypoxia as well as in ErbB2 protein expression in the retina. Additionally, RES plays protective roles in RGCs by promoting cell growth, reducing apoptosis, and decreasing oxidative stress in H2O2-exposed RGCs. RES was also found to inhibit oxidative stress damage in RGCs and suppress the activation of mitogen-activated protein kinase signaling pathways. RES could alleviate retinal function impairment by suppressing the hypoxia-inducible factor-1 alpha/vascular endothelial growth factor and p38/p53 axes while stimulating the PI3K/Akt pathway. Therefore, RES might exert potential therapeutic effects for managing glaucoma by protecting RGCs from damage and promoting their survival.

Resveratrol Inhibits Colorectal Cancer Cell Tumor Property by Activating the miR-769-5p/MSI1 Pathway.

Resveratrol exhibits inhibitory effects on the progression of various cancers including colorectal cancer (CRC), however, the underlying mechanism in regulating CRC development remains elusive. The present study aims to uncover the role and molecular mechanism of resveratrol in modulating CRC cell tumor properties. NCM460 cells, LoVo cells, SW480 cells, and BALB/c nude mice were utilized in this study. RNA levels of miR-769-5p and musashi RNA-binding protein 1 (MSI1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Protein expression was assessed by western blotting or immunohistochemistry assay. Cell viability was analyzed by CCK-8 assay, while cell proliferation and apoptosis were evaluated by 5-Ethynyl-2'-deoxyuridine assay and flow cytometry analysis. Cell migration was investigated by transwell and wound-healing assays. The association between miR-769-5p and MSI1 was identified by a dual-luciferase reporter assay. Tumor formation was analyzed using a xenograft mouse model assay. Compared to control groups, miR-769-5p expression was downregulated, while MSI1 expression was upregulated in CRC tissues and cells. Resveratrol treatment led to increased miR-769-5p expression and decreased MSI1 expression in CRC cells. Resveratrol treatment or miR-769-5p upregulation inhibited CRC cell proliferation and migration, and induced apoptosis. These effects were enhanced after combined treatment with resveratrol and miR-769-5p mimics. MSI1 was identified as a target of miR-769-5p, and its overexpression attenuated the effects of miR-769-5p mimics on cell proliferation, migration, and apoptosis. Moreover, miR-769-5p overexpression enhanced the inhibitory effects of resveratrol on tumor growth in vivo. Resveratrol inhibited colorectal cancer cell tumor properties by activating the miR-769-5p/MSI1 pathway.

Incorporation of Resveratrol-Hydroxypropyl-β-Cyclodextrin Complexes into Hydrogel Formulation for Wound Treatment.

Resveratrol could be applied in wound healing therapies because of its antioxidant, anti-inflammatory and antibacterial effects. However, the main limitation of resveratrol is its low aqueous solubility. In this study, resveratrol was included in hydroxypropyl-β-cyclodextrin complexes and further formulated in Pluronic F-127 hydrogels for wound treatment therapy. IR-spectroscopy and XRD analysis confirmed the successful incorporation of resveratrol into complexes. The wound-healing ability of these complexes was estimated by a scratch assay on fibroblasts, which showed a tendency for improvement of the effect of resveratrol after complexation. The antimicrobial activity of resveratrol in aqueous dispersion and in the complexes was evaluated on methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, and Candida albicans strains. The results revealed a twofold decrease in the MIC and stronger inhibition of the metabolic activity of MRSA after treatment with resveratrol in the complexes compared to the suspended drug. Furthermore, the complexes were included in Pluronic hydrogel, which provided efficient drug release and appropriate viscoelastic properties. The formulated hydrogel showed excellent biocompatibility which was confirmed via skin irritation test on rabbits. In conclusion, Pluronic hydrogel containing resveratrol included in hydroxypropyl-β-cyclodextrin complexes is a promising topical formulation for further studies directed at wound therapy.