Gallic acid exerts anti-inflammatory, anti-oxidative stress, and nephroprotective effects against paraquat-induced renal injury in male rats

2020 ◽  
Vol 394 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Ali Nouri ◽  
Fatemeh Heibati ◽  
Esfandiar Heidarian
2020 ◽  
Vol 58 (1) ◽  
pp. 590-596
Author(s):  
Mohsen Esmaeilzadeh ◽  
Esfandiar Heidarian ◽  
Mehrnoosh Shaghaghi ◽  
Hoshang Roshanmehr ◽  
Mohammad Najafi ◽  
...  

2017 ◽  
Vol 69 (4) ◽  
pp. 830-835 ◽  
Author(s):  
Omid Karimi-Khouzani ◽  
Esfandiar Heidarian ◽  
Sayed Asadollah Amini

Foods ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2872
Author(s):  
Chandra Sekhar Arigela ◽  
Giribabu Nelli ◽  
Siew Hua Gan ◽  
Kuttulebbai Nainamohamed Salam Sirajudeen ◽  
Kumarathevan Krishnan ◽  
...  

Honey has several pharmacological effects, including anti-diabetic activity. However, the effectiveness of bitter gourd honey (BGH) in the treatment of diabetes mellitus (DM) is unknown. The aim of this study was to determine the antioxidant, anti-inflammatory, and anti-apoptotic properties of BGH on the kidney and liver of a streptozotocin-induced diabetes rat model. Methods: A single dose (nicotinamide 110 mg/kg, streptozotocin (STZ) 55 mg/kg, intraperitoneal (i.p.)) was used to induce DM in male rats. For 28 days, normal or diabetic rats were administered 1 g/kg/day and 2 g/kg/day of BGH orally. After the treatment, blood, liver, and kidney samples were collected and analysed for biochemical, histological, and molecular parameters. In addition, liquid chromatography–mass spectrometry (LC-MS) was used to identify the major bioactive components in BGH. Results: The administration of BGH to diabetic rats resulted in significant reductions in alanine transaminase (ALT),aspartate aminotransferase (AST), creatinine, and urea levels. Diabetic rats treated with BGH showed lesser pathophysiological alterations in the liver and kidney as compared to non-treated control rats. BGH-treated diabetic rats exhibited reduced levels of oxidative stress (MDA levels), inflammatory (MYD88, NFKB, p-NFKB, IKKβ), and apoptotic (caspase-3) markers, as well as higher levels of antioxidant enzymes (SOD, CAT, and GPx) in the liver and kidney. BGH contains many bioactive compounds that may have antioxidative stress, anti-inflammatory, and anti-apoptotic effects. Conclusion: BGH protected the liver and kidney in diabetic rats by reducing oxidative stress, inflammation, and apoptosis-induced damage. As a result, BGH can be used as a potential therapy to ameliorate diabetic complications.


Author(s):  
Cristina Bidian ◽  
Daniela-Rodica Mitrea ◽  
Olivia Gabriela Vasile ◽  
Adriana Filip ◽  
Adriana Florinela Cătoi ◽  
...  

Background. The inflammatory mechanisms occur with the highest prevalence in pulmonary pathology. In pharmaceutical industry, carrageenan is used as a pro-inflammatory agent when the activity of anti-inflammatory agents is tested. The oxidative stress represents the imbalance between pro-oxidants and antioxidants which can lead to the activation of the oxidative mechanisms with noxius potential to the body. In experimental studies, quercetin is the most active flavonoid, having the highest anti-inflammatory and antioxidant effects. Curcumin has antioxidant effects that are similar to those of the standard antioxidants and exerts direct anti-inflammatory activity. Aims. The aim of this study is to determine the antioxidant effects of quercetin and curcumin on a carrageenan-induced pleural inflammation. Methods. Eight groups of adult male rats were used: Ia and Ib -control groups, IIa and IIb -with carrageenan administration, IIIa and IIIb -with curcumin and carrageenan, IVa and IVb -with quercetin and carrageenan administration. Blood and lung samples were taken at 4 hours (Ia, IIa, IIIa, IVa groups) and at 24 hours (Ib, IIb, IIIb, IVb groups) after carrageenan administration. Results. In serum, at 4 and at 24 hours, curcumin and quercetin showed protective effects, reducing the oxidative stress (malondialdehyde significantly decreased) and stimulating the antioxidant protection (ceruloplasmin and glutathione significantly increased) in rats with administration of these substances, in comparison to the group that received only carrageenan. In the lungs, at 4 hours, the oxidative stress was significantly reduced only in the rats that received quercetin (malondialdehyde significantly decreased), modifications that were not observed at 24 hours.     Conclusions. In serum, curcumin presented higher antioxidant effects, compared to quercetin. In lungs, quercetin administration showed superior beneficial effects, but only temporarily.


Author(s):  
Mamdooh Ghoneum ◽  
Mohamed S. A. El-Gerbed

Abstract Purpose Methotrexate (MTX) induces hepatotoxicity, limiting its clinical efficacy as a widely known chemotherapy drug. In the current study, we examined the protective effect of human placenta extract (HPE) against MTX-induced liver damage in rats, as well as its ability to regulate antioxidative and anti-inflammatory liver responses. Methods Male rats were orally administered MTX at a daily dose of 5 mg/kg-body-weight in the presence or absence of HPE (10.08 mg/kg) for 2 weeks. We measured the biological effects of MTX and HPE on the levels of liver enzymes, lipid profile, lipid peroxidation, oxidative stress biomarkers, and cytokines [tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10)]. In addition, histological examination and histopathological scoring of liver tissues were performed. Results MTX-treated rats showed significantly increased (p < 0.001) liver enzyme levels for aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, total cholesterol, and triglyceride levels. However, HPE supplementation in MTX-treated rats significantly decreased (p < 0.001) these elevated levels. HPE supplementation also significantly reduced the oxidative stress biomarker malondialdehyde (MDA), reversed the reduction in glutathione (GSH), and markedly increased the antioxidant enzyme activities of catalase (CAT) and superoxide dismutase (SOD) in the livers of MTX-treated rats. Furthermore, HPE supplementation significantly decreased the MTX-elevated levels of the pro-inflammatory cytokines TNF-α, IL-6, and IL-10. Histopathological examinations showed that MTX produced severe cellular damage and inflammatory lesions in liver tissues, while treatment with HPE improved hepatic histologic architecture. Conclusion HPE has the ability to ameliorate methotrexate-induced liver injury in rats by mechanisms that include boosting antioxidative responses and down-regulating MDA and pro-inflammatory cytokine production.


2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Di Feng ◽  
Huanping Zhou ◽  
Xiaohong Jin ◽  
Juan Wei ◽  
Qingqing Zhang ◽  
...  

Electroacupuncture (EA) is reported to possess anti-inflammatory properties and has beneficial effects on acute respiratory distress syndrome (ARDS). However, the underlying mechanisms of the effects of EA on ARDS remain unclear. This study aims to investigate the protective effect of EA on LPS-induced ARDS. In this study, Sprague-Dawley male rats were treated with EA at Hegu (LI4) for 45 minutes before LPS instillation (0.4 mg/kg, 100 ul). H&E staining, wet-to-dry weight (W/D) ratio, PaO2, and protein content in BALF were employed to determine the function of lung tissues. Inflammatory cytokines in serum and BALF were detected by enzyme-linked immunoassay assay (ELISA). The levels of oxidative stress markers were detected to determine the oxidative stress status. Cell apoptosis was observed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and western blot. Here, we found that EA pretreatment effectively alleviated lung pathological damage. Moreover, EA suppressed the oxidative stress damage by upregulating glutathione and superoxide dismutase and downregulating malondialdehyde. EA pretreatment also regulated apoptosis-related proteins, such as Bax and Bcl-2. We found that peroxisome proliferators-activated receptors γ (PPARγ) play a critical role during ARDS, EA up-regulated the expression of PPARγ, which inhibited the activation of nuclear factor-kappa B (NF-κB) and decreased the inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α). When rats were treated with GW9662, a selective PPARγ antagonist, these effects of EA were reversed. Our study demonstrated that EA pretreatment had a beneficial effect on LPS-induced ARDS in rats by anti-inflammatory, antioxidative, and antiapoptotic properties which was regulated via PPARγ/NF-κB signaling pathway.


2010 ◽  
Vol 49 (2) ◽  
pp. 258-267 ◽  
Author(s):  
Chinmay Pal ◽  
Samik Bindu ◽  
Sumanta Dey ◽  
Athar Alam ◽  
Manish Goyal ◽  
...  

2018 ◽  
Vol 96 (4) ◽  
pp. 372-381 ◽  
Author(s):  
Samy Makary ◽  
Mohamed Abdo ◽  
Ereny Fekry

In this study, we aimed to investigate the protective effects of androgens, using letrozole (LET; an aromatase inhibitor), grape seed extract (GSE; a naturally occurring aromatase inhibitor and antioxidant), and testosterone propionate (Tp), against methotrexate (MTX)-induced testicular toxicity in adult male rats. MTX has been shown to induce oxidative stress and exhibit antiproliferative effects in the testes. Adult male rats received oral saline gavage (control group with no treatment), the potential protective agents (LET, GSE, or Tp) alone, MTX alone, or a combination of one of the potential protective agents and MTX. The testicular levels of oxidative stress markers and cytokines (tumor necrosis factor-α and interleukin-1β) were measured. Spermatogenesis and sperm viability were microscopically evaluated. Administration of LET and GSE 7 days before MTX improved spermatogenesis and sperm viability, as well as reduced the levels of oxidative stress markers and cellular cytokines. Exogenous testosterone exhibited anti-inflammatory and antioxidant activities, similar to GSE and LET. We also showed that enhancing the endogenous androgenic activity by LET and GSE protected spermatogenesis against MTX-induced testicular toxicity via reduction of inflammation and oxidative stress in the testes. Our data suggest that testosterone protected spermatogenesis owing to its antioxidant and anti-inflammatory properties.


2020 ◽  
Vol 54 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Samuel Gbadebo Olukole ◽  
Eunice Olufunke Ola-Davies ◽  
Damilare Olaniyi Lanipekun ◽  
Bankole Olusiji Oke

AbstractObjectives. Bisphenol A (BPA) has been reported that among other male reproductive dys-functions, it can cause marked estrogenic effects including alteration in serum hormones as well as testicular lesions in exposed animals. This work sought to study the role of gallic acid (GA), a known antioxidant, on the BPA-induced testicular oxidative stress in adult male Wistar rats using serum hormone analysis, histopathology, and biochemical assays.Methods. Adult male rats were divided into four groups (n=10) including control (0.2 ml of corn oil), GA (20 mg/kg/day), BPA (10 mg/kg/day), BPA+GA (BPA, 10 mg/kg/day + GA, 20 mg/kg/day). All medications were given by oral gavage for 45 consecutive days. The body and testicular weights were measured. Blood and organ samples were collected for the serum hormonal assay: testosterone (T), luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL), and tissue biochemistry analysis: superoxide dismutase (SOD), reduced glutathione (GSH), glutathione-S-transferase (GST), malondialdehyde (MDA), hydrogen peroxide (H2O2), respectively.Results. The BPA-treated rats showed significant reduction in the gonadosomatic index. BPA also caused significant decrease in the levels of the serum testosterone and prolactin. Furthermore, BPA induced testicular oxidative stress by decreasing the activities of antioxidant enzymes and increasing reactive oxygen species. However, co-treatment with GA protected against these alterations.Conclusion. Findings from the present study confirmed the previously reported data and show that the ability of GA, as a potent antioxidant, may protect against BPA-induced alterations in the male reproductive function. Hence, GA protects against testicular oxidative stress in adult male Wistar rats following chronic exposure to BPA.


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