Protective effect of rutin isolated from Spermococe hispida against cobalt chloride-induced hypoxic injury in H9c2 cells by inhibiting oxidative stress and inducing apoptosis

Sundaram.R, Lakshmi; Sali, Veeresh Kumar; Vasanthi, Hannah R.

doi:10.1016/j.phymed.2018.09.229

Cited by 24 publications

(16 citation statements)

References 36 publications

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“…For example, rutin has a strong neuroprotective effect against retinal ganglion cell death induced by hypoxia [16]. A recent study also demonstrates that rutin can alleviate cobalt chloride-induced hypoxia damage by inhibiting oxidative stress and apoptosis in H9c2 cell [17]. Moreover, Liu et al suggest that nobiletin (3′,4′,5,6, 7,8-hexamethoxyflavone) attenuates myocardial I/R injury via activating of Akt/GSK-3β pathway in H9c2 cell [18].…”

Section: Introductionmentioning

confidence: 99%

Norwogonin attenuates hypoxia-induced oxidative stress and apoptosis in PC12 cells

Jing

Gao

Zhang

et al. 2021

BMC Complement Med Ther

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Background Norwogonin is a natural flavone with three phenolic hydroxyl groups in skeletal structure and has excellent antioxidant activity. However, the neuroprotective effect of norwogonin remains unclear. Here, we investigated the protective capacity of norwogonin against oxidative damage elicited by hypoxia in PC12 cells. Methods The cell viability and apoptosis were examined by MTT assay and Annexin V-FITC/PI staining, respectively. Reactive oxygen species (ROS) content was measured using DCFH-DA assay. Lactate dehydrogenase (LDH), malondialdehyde (MDA) and antioxidant enzyme levels were determined using commercial kits. The expression of related genes and proteins was measured by real-time quantitative PCR and Western blotting, respectively. Results We found that norwogonin alleviated hypoxia-induced injury in PC12 cells by increasing the cell viability, reducing LDH release, and ameliorating the changes of cell morphology. Norwogonin also acted as an antioxidant by scavenging ROS, reducing MDA production, maintaining the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), and decreasing the expression levels of HIF-1α and VEGF. In addition, norwogonin prevented cell apoptosis via inhibiting the expression levels of caspase-3, cytochrome c and Bax, while increasing the expression levels of Bcl-2 and the ratio of Bcl-2/Bax. Conclusions Norwogonin attenuates hypoxia-induced injury in PC12 cells by quenching ROS, maintaining the activities of antioxidant enzymes, and inhibiting mitochondrial apoptosis pathway.

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Section: Introductionmentioning

confidence: 99%

Norwogonin attenuates hypoxia-induced oxidative stress and apoptosis in PC12 cells

Jing

Gao

Zhang

et al. 2021

BMC Complement Med Ther

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“…Superoxide anion is rapidly converted by SOD into H 2 O 2 , which is transformed by CAT and GPx into H 2 O 46 . Rutin significantly enhanced activities of SOD, CAT, and GPx in CdCl 2 ‐treated rat brains, cobalt chloride‐treated H9c2 myoblast cells, and endotoxin‐treated injured kidneys and lungs 6,40,47,48 . We propose that pretreatment with rutin raised the activation level of SOD, CAT, and GPx in BisGMA‐treated macrophages.…”

Section: Discussionmentioning

confidence: 80%

“…46 Rutin significantly enhanced activities of SOD, CAT, and GPx in CdCl 2 -treated rat brains, cobalt chloride-treated H9c2 myoblast cells, and endotoxin-treated injured kidneys and lungs. 6,40,47,48 We propose that pretreatment with rutin raised the activation level of SOD, CAT, and GPx in BisGMAtreated macrophages. These results indicated that rutin is able to reduce BisGMA-induced cytotoxicity and genotoxicity through the upregulation of AOE activation.…”

Section: Effects Of Rutin On Bisgma-inhibited Aoe Activities In Rawmentioning

confidence: 84%

Rutin‐protected BisGMA‐induced cytotoxicity, genotoxicity, and apoptosis in macrophages through the reduction of the mitochondrial apoptotic pathway and induction of antioxidant enzymes

Huang

Chang

et al. 2020

Environmental Toxicology

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Bisphenol-A-glycidyldimethacrylate (BisGMA) is a resin monomer frequently used in dentin restorative treatments. The leakage of BisGMA monomer from BisGMA-based polymeric resins can lead to cytotoxicity in macrophages. Rutin has various beneficial bioeffects, including antioxidation and antiinflammation. In this study, we found that pretreatment of RAW264.7 macrophages with rutin-inhibited cytotoxicity induced by BisGMA in a concentration-dependent manner. BisGMA-induced apoptosis, which was detected by levels of phosphatidylserine from the internal to the external membrane and formation of sub-G1, and genotoxicity, which was detected by cytokinesis-blocked micronucleus and single-cell gel electrophoresis assays, were inhibited by rutin in a concentration-dependent manner. Rutin suppressed the BisGMA-induced activation of caspase-3 and-9 rather than caspase-8. Rutin inhibited the activation of the mitochondrial apoptotic pathway, including cytochrome C release and mitochondria disruption, after macrophages were treated with Yin-Che Lu and Yu-Hsiang Kuan contributed equally to this work.

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“…Previous studies have shown that oxidative stress injury causes up-regulation of LDH level and a large accumulation of ROS against SOD activity in cardiomyocytes. 22,23) Other studies have also indicated that luteolin and shengmai injection have antioxidant effects on the oxidative stress injury by up-regulating the HO-1 or CAT mRNA expression level in rat cardiomyocytes. 24,25) These are consistent with the results of the present study.…”

Section: Discussionmentioning

confidence: 99%

Qiliqiangxin Attenuates Oxidative Stress-Induced Mitochondrion-Dependent Apoptosis in Cardiomyocytes <i>via</i> PI3K/AKT/GSK3β Signaling Pathway

Zhao

Chang

et al. 2019

Biological & Pharmaceutical Bulletin

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Qiliqiangxin capsule (QLQX) is a well-known traditional Chinese medicine that exhibits cardioprotective effects in heart failure patients. However, it remains unclear whether and by which mechanism QLQX attenuates oxidative stress-induced mitochondria-dependent myocardial apoptosis. In vivo, Sprague Dawley (SD) rats received left anterior descending coronary artery ligation for 4 weeks to establish a model of heart failure after acute myocardial infarction, and then were treated with QLQX for another 4 weeks. We evaluated cardiac function, oxidative stress injury, as well as the expressions of mitochondria-dependent apoptosis and its signaling factors. The results indicated that QLQX protected cardiac function and attenuated oxidative stress-induced myocardial apoptosis. Meanwhile, QLQX elevated the Bcl-2 expression, declined the expressions of Bax, cytochrome c, apoptotic protease activating factor-1 (Apaf-1), cleaved-caspase 9 and cleaved-caspase 3, and up-regulated the ratios of phospho-AKT/AKT and phospho-glycogen synthase kinase-3β (GSK3β)/GSK3β. In vitro, H9c2 cardiomyocytes were pretreated with QLQX, then exposed to H 2 O 2 for 24 h. QLQX promoted the proliferation of H9c2 cardiomyocytes induced by H 2 O 2 and reversed oxidative stress damage. Moreover, QLQX inhibited the apoptosis rate and the pro-apoptosis protein expressions, but improved the Bcl-2 expression as well as the ratios of phospho-AKT/AKT and phospho-GSK3β/ GSK3β. Meanwhile, it further ameliorated mitochondrion-related apoptosis by inhibiting the mitochondrial fission, mitochondrial permeability transition pore (MPTP) opening, and mitochondrial membrane potential (MMP) decline in H9c2 cardiomyocytes induced by H 2 O 2. In addition, all the effects of QLQX on H 2 O 2-induced mitochondria-dependent apoptosis could be blocked by the phosphoinositide 3-kinase (PI3K) inhibitor, LY294002. We conclude that QLQX may ameliorate oxidative stress-induced mitochondria-dependent apoptosis in cardiomyocytes through PI3K/AKT/GSK3β signaling pathway.

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Protective effect of rutin isolated from Spermococe hispida against cobalt chloride-induced hypoxic injury in H9c2 cells by inhibiting oxidative stress and inducing apoptosis

Cited by 24 publications

References 36 publications

Norwogonin attenuates hypoxia-induced oxidative stress and apoptosis in PC12 cells

Norwogonin attenuates hypoxia-induced oxidative stress and apoptosis in PC12 cells

Rutin‐protected BisGMA‐induced cytotoxicity, genotoxicity, and apoptosis in macrophages through the reduction of the mitochondrial apoptotic pathway and induction of antioxidant enzymes

Qiliqiangxin Attenuates Oxidative Stress-Induced Mitochondrion-Dependent Apoptosis in Cardiomyocytes <i>via</i> PI3K/AKT/GSK3β Signaling Pathway

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