scholarly journals Insight into the Protective Effect of Salidroside against H2O2-Induced Injury in H9C2 Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Hui Gao ◽  
Xueping Liu ◽  
Kunming Tian ◽  
Yichong Meng ◽  
Cuicui Yu ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect ◽  
Underlying Mechanism ◽  
Antioxidant Enzyme Activities ◽  
H9c2 Cells ◽  
H2o2 Treatment ◽  
P53 Overexpression ◽  
Intracellular Ros ◽  
Wide Range ◽  
Related Proteins

Salidroside is the important active ingredient of Rhodiola species, which shows a wide range of pharmacological activities such as antioxidative stress, anti-inflammation, and antiliver fibrosis. In this paper, we aimed to study the protective effect and mechanism of salidroside against H2O2-induced oxidative damage in H9C2 cells by determining cell proliferation rate, intracellular reactive oxygen species (ROS) level, antioxidant enzyme activities, and the expression of apoptosis-related proteins. The results showed that salidroside significantly alleviated cell growth inhibition induced by H2O2 treatment in H9C2 cells, decreased the levels of intracellular ROS and malondialdehyde (MDA), and increased the activity of superoxide dismutase (SOD) and catalase (CAT); meanwhile, salidroside upregulated the expression of Bcl-2 while downregulated the expression of Bax, p53, and caspase-3 in H2O2-treated H9C2 cells. Furthermore, the antiapoptotic effect of salidroside was almost eliminated by the knockdown of Bcl-2. In the further exploration, the Bcl-2 expression was decreased by the p53 overexpression and increased by p53 knockdown in H2O2-treated H9C2 cells. Consequently, salidroside could protect H9C2 cells against H2O2-induced oxidative damage, and the underlying mechanism may be related to scavenging intracellular ROS, increasing the activities of intracellular antioxidant enzymes and inhibiting the expression of apoptosis-related proteins.

scholarly journals SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhiya Deng ◽  
Maomao Sun ◽  
Jie Wu ◽  
Haihong Fang ◽  
Shumin Cai ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Cell Model ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Autophagy Induction ◽  
Promising Therapeutic Approach ◽  
Related Proteins ◽  
Caecal Ligation And Puncture

AbstractOur previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.

scholarly journals t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

Dose-Response ◽  
2018 ◽  
Vol 16 (3) ◽  
pp. 155932581879630 ◽  
Author(s):  
Graciela Gavia-García ◽  
María de los Ángeles Rosas-Trejo ◽  
Eduardo García-Mendoza ◽  
Rafael Toledo-Pérez ◽  
Mina Königsberg ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect ◽  
Antioxidant Response ◽  
Nuclear Factor Κb ◽  
Pharmacological Intervention ◽  
Antioxidant Enzyme Activities ◽  
Lactation Period ◽  
Oxidative Protein Damage ◽  
Lower Protein ◽  
Antioxidant Mechanisms

Objective: Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated. Methods: Malnutrition in pops-rats was induced during the lactation period and first-, second-, and third-degree malnourished rats were studied (MN1, MN2, and MN3). To determine t-BHQ protective effect, lipid peroxidation (LPx) was assessed, as well as the carbonyl content. The reduced glutathione and glutathione disulfide content were determined and antioxidant enzyme activities were measured. Results: Oxidative protein damage, LPx, and Nuclear Factor-κB (NF-κB) content, increased in the MN2 and MN3 compared to well-nourished rats, associated with lower protein content and antioxidant activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase. Tert-butylhydroquinone treatment induced a protective effect against lipids and proteins oxidative damage, as well as decrease in NF-κB in MN rats and restored the antioxidant mechanisms, mostly GPx and SOD. No differences were found between male and female animals. Conclusions: Results show that higher body weight deficit leads to increased oxidative damage and probably inflammation, attributable to alterations in antioxidant mechanisms. These effects were reversed by the t-BHQ-treatment, which restores the antioxidant response. Our findings suggest that t-BHQ could be an interesting pharmacological intervention, but it needs to be studied further.

scholarly journals Antioxidant Properties of UnripeCarica papayaFruit Extract and Its Protective Effects against Endothelial Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Wattanased Jarisarapurin ◽  
Wariya Sanrattana ◽  
Linda Chularojmontri ◽  
Khwandow Kunchana ◽  
Suvara K. Wattanapitayakul
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Cell Survival ◽  
Antioxidant Properties ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Ros Scavenging ◽  
Tropical Fruit ◽  
Intracellular Ros ◽  
High Antioxidant Activity

It has been proven that high consumption of fruit and vegetable lowers the risks of cardiovascular and other oxidative stress-related diseases. Here we evaluated the effects of a tropical fruit, unripeCarica papaya(UCP), on endothelial protection against oxidative damage induced by H2O2. The antioxidant properties of UCP were investigated using the assays of FRAP and ORAC and specific ROS scavenging activities (H2O2,O2•-, OH•, HOCl). Cytoprotective property was tested in human endothelial cell line EA.hy926 with respect to cell survival, intracellular ROS levels, antioxidant enzyme activities (CAT, SOD, GPX), survival/stress signaling (AKT, JNK, p38), and nuclear signaling (Nrf2, NF-kB). UCP processed high antioxidant activity and scavenging activity against H2O2> OH•>O2•-> HOCl, respectively. UCP improved cell survival in the milieu of ROS reduction. While SOD was increased by UCP, CAT activity was enhanced when cells were challenged with H2O2. UCP had no impact on H2O2-activated AKT, JNK, and p38 signaling but significantly decreased nuclear NF-κB levels. The overactivation of Nrf2 in response to oxidative stress was constrained by UCP. In conclusion, UCP protected endothelial cells against oxidative damage through intracellular ROS reduction, enhanced CAT activity, suppression of NF-kB, and prohibition of Nrf2 dysregulation. Thus, UCP might be a candidate for development of nutraceuticals against CVD and oxidative-related diseases and conditions.

scholarly journals Protective effect of procyanidin B2 on hydrogen peroxide (H2O2)-induced oxidative damage in MCF-7 cells

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Jia-qi Tan ◽  
Peng-cheng Li ◽  
Qian Li ◽  
Jin-tian Tang ◽  
Hong-kun Xue
Keyword(s):  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Molecular Mechanisms ◽  
Antioxidant Properties ◽  
Expression Levels ◽  
Diphenyltetrazolium Bromide ◽  
Antioxidant Enzymes Activities ◽  
Related Proteins ◽  
Mcf 7

Abstract The aim of this study is to assess the cytoprotection and potential molecular mechanisms of procyanidin B2 (PCB2) on hydrogen peroxide (H2O2)-induced oxidative damage in MCF-7 cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to determine the viability of MCF-7 cell exposure to H2O2 or PCB2. We measured the antioxidant properties of PCB2 by determining the activities of SOD, GSH-Px, LDH and MDA levels, and evaluated apoptosis and intracellular reactive oxygen species (ROS) levels. The related proteins expression levels were monitored by Western blot. MCF-7 cells induced with H2O2 had a remarkable decrease in cell viability that was suppressed when it was interfered with PCB2 (0.1–10.0 μM). PCB2 interference memorably and dose-dependently inhibited H2O2-induced LDH leakage, ROS and MDA overproduction, while PCB2 markedly increased H2O2-induced the activities of SOD and GSH-Px. Eventually, H2O2 prominently down-regulated the ratio of Bcl-2/Bax and the relative proteins expression levels of Nrf2, GCLC, NQO1 and HO-1, and up-regulated the relative proteins expression levels of cytochrome c, caspase-3 and Keap1. However, the relative expression levels of these proteins were reversed in PCB2-interfered MCF-7 cells. This study implied that protective effect of PCB2 on H2O2-induced oxidative damage in MCF-7 cells might be related to inhibition of mitochondria-dependent apoptosis, activation of Keap1/Nrf2/HO-1 signaling pathway and improvement of the antioxidant enzymes activities.

Protective effect of chitooligosaccharides on hydrogen peroxide-induced PC-12 cells death by inhibition of oxidative damage

2010 ◽  
Vol 34 (8) ◽  
pp. S27-S27
Author(s):  
Xueling Dai ◽  
Ping Chang ◽  
Ke Xu ◽  
Changjun Lin ◽  
Hanchang Huang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Pc 12 Cells ◽  
Cells Death

Melatonin protects against cadmium-induced oxidative damage in different tissues of rat: a mechanistic insight

2019 ◽  
Vol 2 (2) ◽  
pp. 1-21 ◽  
Author(s):  
Elina Mitra ◽  
Bharati Bhattacharjee ◽  
Palash Kumar Pal ◽  
Arnab Kumar Ghosh ◽  
Sanatan Mishra ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Oxidative Damage ◽  
Protein Carbonyl ◽  
Environmental Pollutant ◽  
Glutathione S Transferase ◽  
Protein Carbonyl Content ◽  
Wide Range ◽  
Liver And Kidney ◽  
Nadh Cytochrome ◽  
Cd Exposure

Cadmium (Cd) is a notorious environmental pollutant known for its wide range of toxicities to organisms. Thus, the present study is designed to examine whether melatonin, a potent antioxidant, protects against Cd-induced oxidative damage in the heart, liver and kidney of rats. Cd treatment at a dose of 0.44 mg/kg for 15 days caused severe damage in all these organs. These included significantly increased activities of SGPT, SGOT, lactate dehydrogenase- 1 and 5 and ALP and levels of total lactate, creatinine, lipid peroxidation, protein carbonyl content and reduced glutathione while the activities of superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase along with mitochondrial pyruvate dehydrogenase, isocitrate dehydrogenase, α-keto glutarate dehydrogenase, succinate dehydrogenase, NADH-cytochrome-c-oxidoreductase and cytochrome-c-oxidase were significantly reduced by Cd. However, if melatonin was given orally 30 min before Cd injection, all these alterations induced by Cd were significantly preserved by melatonin. Histological observations also demonstrated that Cd exposure caused cellular lesions, promoting necrotic or apoptotic changes. Notably, all these changes were significantly protected by melatonin. The results suggest that melatonin is a beneficial molecule to ameliorate Cd-induced oxidative damage in the heart, liver and kidney tissues of rats with its powerful antioxidant capacity, heavy metal chelating activity and competition of binding sites with Cd to the GSH and catalase.

Protective Effect of Chungkukjang from Sunchang Province against Cellular Oxidative Damage

2008 ◽  
Vol 13 (2) ◽  
pp. 90-94 ◽  
Author(s):  
Ji-Myung Choi ◽  
Na-Ri Yi ◽  
Kyoung-Chun Seo ◽  
Ji-Sook Han ◽  
Young-Ok Song ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect

Testicular Injury Attenuated by Rapamycin Through Induction of Autophagy and Inhibition of Endoplasmic Reticulum Stress in Streptozotocin- Induced Diabetic Rats

2019 ◽  
Vol 19 (5) ◽  
pp. 665-675 ◽  
Author(s):  
Wenjiao Shi ◽  
Zhixin Guo ◽  
Ruixia Yuan
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Protective Effect ◽  
Er Stress ◽  
B Cell Lymphoma ◽  
Diabetic Rats ◽  
Pathological Changes ◽  
Rapamycin Treatment ◽  
Related Proteins

Background and Objective: This study investigated whether rapamycin has a protective effect on the testis of diabetic rats by regulating autophagy, endoplasmic reticulum stress, and oxidative stress. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups: control, diabetic, and diabetic treated with rapamycin, which received gavage of rapamycin (2mg.kg-1.d-1) after induction of diabetes. Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65mg.Kg-1). All rats were sacrificed at the termination after 8 weeks of rapamycin treatment. The testicular pathological changes were determined by hematoxylin and eosin staining. The protein or mRNA expression of autophagy-related proteins (Beclin1, microtubule-associated protein light chain 3 (LC3), p62), ER stress marked proteins (CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), caspase-12), oxidative stress-related proteins (p22phox, nuclear factor erythroid2-related factor 2 (Nrf2)) and apoptosis-related proteins (Bax, B cell lymphoma-2 (Bcl-2)) were assayed by western blot or real-time fluorescence quantitative PCR. Results: There were significant pathological changes in the testes of diabetic rats. The expression of Beclin1, LC3, Nrf2, Bcl-2 were significantly decreased and p62, CHOP, caspase12, p22phox, and Bax were notably increased in the testis of diabetic rats (P <0.05). However, rapamycin treatment for 8 weeks significantly reversed the above changes in the testis of diabetic rats (P <0.05). Conclusion: Rapamycin appears to produce a protective effect on the testes of diabetic rats by inducing the expression of autophagy and inhibiting the expression of ER-stress, oxidative stress, and apoptosis.

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