Cardioprotective effects of anisodamine against myocardial ischemia/reperfusion injury through the inhibition of oxidative stress, inflammation and apoptosis

Yao, Bao‐Ju; He, Xiaoqing; Lin, Yani; Dai, Wenjun

doi:10.3892/mmr.2017.8009

Cited by 22 publications

(22 citation statements)

References 26 publications

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“…The mice were randomly divided into four groups (n = 5): Control group, ANIdown-regulating the expression of caspase 3 and Bax. 10,12 In addition, the combination of ANI and neostigmine improved acute fatal crush syndrome by activating α 7 nicotine acetylcholine receptor (α 7nAChR)-dependent JAK2-STAT3 pathway. 27 Surprisingly, the anti-inflammatory effect of ANI was also found to be applicable to tumor progression in this study.…”

Section: Discussionmentioning

confidence: 99%

“…9 ANI has also been reported to have a significant anti-inflammatory effect, which can alleviate the damage of kidney and heart by inhibiting the activation of inflammasomes and the expression of inflammatory factors. 10,11 Similarly, ANI showed an anti-apoptotic effect in myocardial ischemic injury. 12 However, the role of ANI in tumors has not been revealed.…”

Section: Introductionmentioning

confidence: 96%

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<p>Anisodamine Suppressed the Growth of Hepatocellular Carcinoma Cells, Induced Apoptosis and Regulated the Levels of Inflammatory Factors by Inhibiting NLRP3 Inflammasome Activation</p>

Liu

2020

DDDT

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Introduction: Hepatocellular carcinoma (HCC) is a primary liver cancer with a 5-year incidence of over 70%. Anisodamine (ANI), an alkaloid extracted from Anisodus, has a good therapeutic effect in septic shock and morphine addiction. Our study designed to investigate the anticancer effect of anisodamine (ANI) on HCC. Materials and Methods: HepG2 cells were subcutaneously injected into BALB/C nude mice and the tumor tissue was subcutaneously inoculated to construct the transplanted tumor. Mice were randomly divided into 10 groups (n = 5): control group, ANI-10 group, ANI-50 group, ANI-200 group, ANI-200+pcDNA-NLRP3 group, ANI-200+EV group, sh-NLRP3 group, ANI-200 + sh-NLRP3 group, normal group and normal+ANI-200 group. Results: Studies indicated that ANI inhibited the growth of HCC xenografts and reduced liver damage in a dose-dependent manner. Besides, ANI increased the survival rate of tumorbearing mice and suppressed the expression of NLRP3 in a dose-dependent manner. It is worth noting that NLRP3 overexpression reversed the inhibitory effect of ANI on HCC xenografts. In addition, TUNEL analysis showed that ANI-induced apoptosis of tumor cells, and NLRP3 overexpression reversed the inhibitory effect of ANI on HCC. Moreover, ANI further regulated the levels of IFN-γ, TNF-α, IL-4 and IL-27. Notably, low expression of NLRP3 enhanced the inhibitory effect of ANI on the development of HCC xenografts in mice. Discussion: These findings indicate that ANI suppressed the growth of HCC cells, induced apoptosis and regulated the levels of inflammatory factors by inhibiting NLRP3 inflammasome activation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

<p>Anisodamine Suppressed the Growth of Hepatocellular Carcinoma Cells, Induced Apoptosis and Regulated the Levels of Inflammatory Factors by Inhibiting NLRP3 Inflammasome Activation</p>

Liu

2020

DDDT

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“…Ischemia-reperfusion injury is accepted as one of the contributors to many cardiovascular diseases by bringing irreversible damage to the endothelium by inducing cell apoptosis and inflammation [ 15 ]. The inflammatory cytokines generated in vivo by ischemia-reperfusion injury would recruit immune cells, which would further participate in exacerbating blood vessel barrier dysfunction by direct inflammatory cell infiltration and promoting thrombosis by activating circulating platelets [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Emodin, A Chinese Herbal Medicine, Inhibits Reoxygenation-Induced Injury in Cultured Human Aortic Endothelial Cells by Regulating the Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) and Endothelial Nitric Oxide Synthase (eNOS) Signaling Pathway

et al. 2018

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BackgroundIschemia-reperfusion injury is associated with vascular dysfunction. The aim of this study was to investigate the role of emodin, a Chinese herbal medicine, in hypoxia-reoxygenation injury in cultured human aortic endothelial cells (HAECs) and its effects on the expression of the peroxisome proliferator-activated receptor-γ (PPAR-γ) and endothelial nitric oxide synthase (eNOS) signaling pathway.Material/MethodsAn in vitro hypoxia-reoxygenation model used cultured human aortic endothelial cells (HAECs). A colorimetric method evaluated the activity of peroxisome proliferator-activated receptor-γ (PPAR-γ). Phosphorylation of PPAR-γ and endothelial nitric oxide synthase (eNOS) were measured by Western blotting. Expression of inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 were evaluated by enzyme-linked immunosorbent assay (ELISA) and Western blotting. Nitric oxide (NO) production was detected by diaminofluorescein-FM diacetate (DAF-FM DA) fluorescence. Immunoprecipitation was used to evaluate the molecular coupling of heat shock protein (HSP)90 and eNOS.ResultsHypoxia-reoxygenation injury of HAECs reduced the activity and phosphorylation of PPAR-γ, and eNOS, NO production, and HSP90/eNOS molecular coupling in a time-dependent manner. Hypoxia-reoxygenation increased the levels of inflammatory cytokines TNF-α, IL-6, and IL-8 in a time-dependent manner. Emodin treatment recovered PPAR-γ activity and phosphorylation, eNOS phosphorylation, and HSP90/eNOS coupling in HAECS in a concentration-dependent manner, which was reversed by the PPAR-γ inhibitor GW9662, and the eNOS inhibitor, L-NAME. The recovery of HSP90/eNOS coupling by emodin was impaired by GW9662 treatment.ConclusionsAn in vitro hypoxia-reoxygenation (ischemia-reperfusion injury) model of induction of endothelial cell inflammatory mediators showed that emodin recovered the PPAR-γ and eNOS pathway activity.

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“…Studies have shown that myocardial cell damage is closely related to Oxidative Stress (OS) and inflammation [7]. OS refers to an unbalanced state caused by excessive oxidation of the body.…”

Section: Protective Mechanism Of Xinmailong Injection On Cardiomentioning

confidence: 99%

Intervention Mechanisms of Xinmailong Injection, a Periplaneta Americana Extract, on Cardiovascular Disease: A Systematic Review of Basic Researches

Lin

Liu

Wang

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Background. At present, the prevention and treatment of cardiovascular disease in the world are facing severe challenges. Xinmailong injection, which is derived from the animal medicine Periplaneta Americana, has certain advantages in the clinical treatment of cardiovascular disease. This study systematically evaluated the basic research reports of Xinmailong Injection on cardiovascular disease and made its pharmacological mechanisms more clear. Methods. Basic research reports on the intervention mechanisms of Xinmailong Injection on cardiovascular disease in PubMed, EMBASE, Cochrane Library (No. 2, 2019), CNKI, Wan Fang, and VIP databases were searched. The search time limit was from the establishment of the database to February 2019. The literature was screened according to inclusion and exclusion criteria, and then the data were extracted and a descriptive analysis of the pharmacological mechanisms of Xinmailong Injection on cardiovascular disease was performed. Results. Finally, twenty-two basic research reports were included. The intervention mechanisms of Xinmailong Injection on cardiovascular disease mainly includes the following: inhibiting oxidative stress and inflammatory reaction; regulating autophagy; promoting Ca2+ influx by activating excitability of excitation-contraction coupling (ECC); inhibiting overexpressions of transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) to regulate the dynamic balance of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs); inhibiting the phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2), protein kinase B (AKT), and glycogen synthase kinase 3β (GSK3β) proteins and overexpression of the downstream transcription factor GATA4 in the nucleus; regulating vascular endothelial factors and so on. Conclusions. Xinmailong Injection can protect cardiomyocytes and maintain the normal function of the heart in various ways, thus effectively preventing the development of cardiovascular disease. Therefore, Xinmailong Injection has great potential for clinical application, and more basic researches need to be carried out to explore the medicinal value of Xinmailong Injection.

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Cardioprotective effects of anisodamine against myocardial ischemia/reperfusion injury through the inhibition of oxidative stress, inflammation and apoptosis

Cited by 22 publications

References 26 publications

<p>Anisodamine Suppressed the Growth of Hepatocellular Carcinoma Cells, Induced Apoptosis and Regulated the Levels of Inflammatory Factors by Inhibiting NLRP3 Inflammasome Activation</p>

<p>Anisodamine Suppressed the Growth of Hepatocellular Carcinoma Cells, Induced Apoptosis and Regulated the Levels of Inflammatory Factors by Inhibiting NLRP3 Inflammasome Activation</p>

Emodin, A Chinese Herbal Medicine, Inhibits Reoxygenation-Induced Injury in Cultured Human Aortic Endothelial Cells by Regulating the Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) and Endothelial Nitric Oxide Synthase (eNOS) Signaling Pathway

Intervention Mechanisms of Xinmailong Injection, a Periplaneta Americana Extract, on Cardiovascular Disease: A Systematic Review of Basic Researches

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