Tongmai Yangxin pill reduces myocardial no-reflow by regulating apoptosis and activating PI3K/Akt/eNOS pathway

Chen, Rui; Chen, Ting; Wang, Tianqi; Dai, Xiangdong; Meng, Ke; Zhang, Shuying; Jiang, Di; Wang, Yanyan; Zhou, Kun; Geng, Tao; Xu, Jianqing; Wang, Yi

doi:10.1016/j.jep.2020.113069

Cited by 16 publications

(14 citation statements)

References 21 publications

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“…eNOS activity is mainly regulated through phosphorylation, which is primarily regulated by the PI3K/Akt/eNOS pathway. It has been reported that activation of PI3K/AKT/eNOS pathways serves an important role in regulating cell migration, migration, angiogenesis and apoptosis ( 46 ). The results of the present study showed that HSYA may rescue NO production in CRF serum-treated cells via inhibiting PI3K/Akt activation.…”

Section: Discussionmentioning

confidence: 99%

Hydroxysafflor Yellow A inhibits the viability and migration of vascular smooth muscle cells induced by serum from rats with chronic renal failure via inactivation of the PI3K/Akt signaling pathway

Huo¹,

Wang²,

Wang³

et al. 2021

Exp Ther Med

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It has been reported that the viability and migration of vascular smooth muscle cells contributes to arteriovenous fistula stenosis. Hydroxysafflor Yellow A (HSYA) has been demonstrated to inhibit the viability and migration of VSMCs by regulating Akt signaling. The present study aimed to investigate the role of HSYA on the viability and migration of human umbilical vein smooth muscle cells (HUVSMCs) following stimulation using serum from rats with chronic renal failure (CRF), and to determine the effects of HSYA on PI3K/Akt signaling. Wistar rats were randomly divided into two groups, control and CRF groups. Serum from each group was collected to stimulate the HUVSMCs. Cell Counting Kit-8 and wound healing assays were performed to assess cell viability and migration, respectively. Flow cytometry analysis was performed to assess apoptosis, and western blot analysis was performed to detect protein expression levels of PI3K and Akt. Nitric oxide (NO) production was measured using the Nitrate/Nitrite assay kit. The results demonstrated that serum from CRF rats significantly enhanced cell viability, migration and apoptosis, the effects of which were reversed following treatment with HSYA. In addition, CRF serum decreased NO and endothelial NO synthase expression, whilst increasing the protein expression levels of PI3K and phosphorylated-Akt in HUVSMCs. Notably, treatment with HSYA markedly restored NO production and inactivated the PI3K/Akt signaling pathway. Furthermore, the PI3K/Akt inhibitor, AMG511, exerted similar effects to HSYA. Taken together, the results of the present study suggest that HSYA suppresses cell viability and migration in the presence of CRF serum by inactivating the PI3K/Akt signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Hydroxysafflor Yellow A inhibits the viability and migration of vascular smooth muscle cells induced by serum from rats with chronic renal failure via inactivation of the PI3K/Akt signaling pathway

Huo¹,

Wang²,

Wang³

et al. 2021

Exp Ther Med

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“…For example, phosphatase PTEN that negatively regulates the PI3K/Akt pathway can be inhibited by ROS [234,235], exosomes derived from bone marrow stromal cells [236], or Achyranthes bidentata polypeptides [237], then enhancing Akt phosphorylation and promoting myocardial protection. Treatments targeting PI3K/Akt or related signaling pathways reduce reperfusion complications such as arrhythmias [238,239], myocardial stunning [239], myocardial no-reflow [240], and adverse remodeling [241]. [19,[91][92][93][94].…”

Section: Regulation Of the Oxidation Defense Systemmentioning

confidence: 99%

Role of Oxidative Stress in Reperfusion following Myocardial Ischemia and Its Treatments

Xiang

Xin

et al. 2021

Oxidative Medicine and Cellular Longevity

138

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Myocardial ischemia is a disease with high morbidity and mortality, for which reperfusion is currently the standard intervention. However, the reperfusion may lead to further myocardial damage, known as myocardial ischemia/reperfusion injury (MI/RI). Oxidative stress is one of the most important pathological mechanisms in reperfusion injury, which causes apoptosis, autophagy, inflammation, and some other damage in cardiomyocytes through multiple pathways, thus causing irreversible cardiomyocyte damage and cardiac dysfunction. This article reviews the pathological mechanisms of oxidative stress involved in reperfusion injury and the interventions for different pathways and targets, so as to form systematic treatments for oxidative stress-induced myocardial reperfusion injury and make up for the lack of monotherapy.

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“…Ni induced intrinsic mitochondrial apoptosis via up-regulation of cytochrome c, caspase-9 and cleaved caspase-3, and down-regulation of Bcl-2, which could be alleviated by Nano-Se both in vitro and in vivo, clearly suggesting that Nano-Se could perform hepatoprotection effects via inhibiting mitochondrial pathway. PI3K/Akt signaling pathway plays an essential role in cell growth, migration, proliferation, metabolism, and apoptosis activation, which is associated with Bcl-2 family proteins 47,48. Study indicated that excessive NiCl 2 decreased the expression of Bcl-2 and Bcl-xL and increased the expression of Bax and BAK, resulting in renal tubular apoptosis by inhibiting PI3K/Akt pathway in chicken 4.…”

mentioning

confidence: 99%

Nano‐selenium attenuates mitochondrial‐associated apoptosis via the PI3K/AKT pathway in nickel‐induced hepatotoxicity in vivo and in vitro

Wang

et al. 2021

Environmental Toxicology

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The aim of this study was to investigate the protective effects of Nano-Se against nickel (Ni)-induced hepatotoxicity and the potential mechanism. Hence, we constructed in vivo and in vitro models of Ni-induced hepatotoxicity. Sprague-Dawley (SD) rats were exposed to nickel sulfate (NiSO 4 , 5.0 mg/kg, i.p.) with or without Nano-Se (0.5, 1, and 2 mg/kg, oral gavage) co-administration for 14 days, and HepG2 cells were exposed to NiSO 4 (1500 μM) with or without Nano-Se (20 μM) for 24 h. Nano-Se obviously prevented Ni-induced hepatotoxicity indicated by ameliorating pathological change and decreasing Ni accumulation in rat livers. Ni induced a significant increase in hepatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GSH-Px), and malondialdehyde (MDA) level, decreased the glutathione (GSH) content while compared to those in the control group. Nano-Se administration improved the hepatic antioxidant capacity through increase hepatic GSH contents and GSH-Px activity, decrease the activities of SOD, CAT, and MDA level. Nano-Se improved the cell viability, decreased active oxygen (ROS) generation and ameliorated morphological changes of nuclear structures in Ni-treated HepG2 cells. In addition, Nano-Se inhibited the Ni-induced increases of cytochrome c, caspase-9, cleaved caspase-3, increased PI3K and AKT phosphorylation both in vivo and in vitro. Besides, the PI3K inhibitor Y294002 could inhibit the protective effects of Nano-Se on apoptosis. Thus, Nano-Se significantly activates PI3K/AKT signaling to ameliorate apoptosis in Ni-induced hepatotoxicity.

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Tongmai Yangxin pill reduces myocardial no-reflow by regulating apoptosis and activating PI3K/Akt/eNOS pathway

Cited by 16 publications

References 21 publications

Hydroxysafflor Yellow A inhibits the viability and migration of vascular smooth muscle cells induced by serum from rats with chronic renal failure via inactivation of the PI3K/Akt signaling pathway

Hydroxysafflor Yellow A inhibits the viability and migration of vascular smooth muscle cells induced by serum from rats with chronic renal failure via inactivation of the PI3K/Akt signaling pathway

Role of Oxidative Stress in Reperfusion following Myocardial Ischemia and Its Treatments

Nano‐selenium attenuates mitochondrial‐associated apoptosis via the PI3K/AKT pathway in nickel‐induced hepatotoxicity in vivo and in vitro

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