Effect and mechanism of asiatic acid on autophagy in myocardial ischemia‑reperfusion injury &lt;em&gt;in&amp;nbsp;vivo&lt;/em&gt; and &lt;em&gt;in&amp;nbsp;vitro&lt;/em&gt;

Yi, Chenlong; Si, Linjie; Xu, Jing; Yang, Junyi; Wang, Qiang; Wang, Xiaowei

doi:10.3892/etm.2020.9182

Cited by 18 publications

(21 citation statements)

References 54 publications

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“…As a traditional Chinese medicine, AA exerts beneficial effects on oxidative stress in many disease models. In our previous study, we found that AA reduced ROS generation during MIRI and inhibited excess autophagy [ 18 ]. The results of the current study suggest that oxidative stress-induced injury plays a significant role in MIRI.…”

Section: Discussionmentioning

confidence: 99%

“…In a hepatic I-R injury model, the protective effect of AA was achieved by increasing the expression of peroxisome proliferator-activated receptor gamma (PPAR γ ) and ultimately attenuating the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome [ 17 ]. Pharmacological studies of AA in MIRI have also been documented [ 18 , 19 ], but its mechanism remains ambiguous. In the current study, we combined in vivo and in vitro models to explore additional mechanisms of AA during MIRI and aimed to prove the potential pharmacological properties of AA in the clinical treatment of CHD.…”

Section: Introductionmentioning

confidence: 99%

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Asiatic Acid Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting the ROS-Mediated Mitochondria-Dependent Apoptosis Pathway

Song

Sun

et al. 2022

Oxidative Medicine and Cellular Longevity

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Myocardial ischemia-reperfusion injury (MIRI) is a major cause of heart failure in patients with coronary heart disease (CHD). Mitochondrial dysfunction is the crucial factor of MIRI; oxidative stress caused by mitochondrial reactive oxygen species (ROS) aggravates myocardial cell damage through the mitochondria-dependent apoptosis pathway. Asiatic acid (AA) is a type of pentacyclic triterpene compound purified from the traditional Chinese medicine Centella asiatica, and its protective pharmacological activities have been reported in various disease models. This study is aimed at investigating the protective effects of AA and the underlying mechanisms in MIRI. To achieve this goal, an animal model of MIRI in vivo and a cell model of oxygen-glucose deprivation/reperfusion (OGD/R) in vitro were established. The results show that AA exerts a protective effect on MIRI by improving cardiac function and reducing cardiomyocyte damage. Due to its antioxidant properties, AA alleviates mitochondrial oxidative stress, as evidenced by the stable mitochondrial structure, maintained mitochondrial membrane potential (MMP), and reduced ROS generation, otherwise due to its antiapoptotic properties. AA inhibits the mitogen-activated protein kinase (MAPK)/mitochondria-dependent apoptosis pathway, as evidenced by the limited phosphorylation of p38-MAPK and JNK-MAPK, balanced proportion of Bcl-2/Bax, reduced cytochrome c release, inhibition of caspase cascade, and reduced apoptosis. In conclusion, our study confirms that AA exerts cardiac-protective effects by regulating ROS-induced oxidative stress via the MAPK/mitochondria-dependent apoptosis pathway; the results provide new evidence that AA may represent a potential treatment for CHD patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Asiatic Acid Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting the ROS-Mediated Mitochondria-Dependent Apoptosis Pathway

Song

Sun

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…It is generally believed that Beclin-1-mediated autophagy is not only regulated by its own expression, but is also promoted by the binding of Beclin-1 and Bcl-2 ( Marquez and Xu, 2012 ). Previous studies have shown that the balance between Bcl-2 and Beclin-1 protein expression affects the levels of autophagy ( Yi et al, 2020 ). We therefore explored the association between Bcl-2 and Beclin-1 protein expression in the crosstalk between apoptosis and autophagy in rat heart after I/R injury.…”

Section: Discussionmentioning

confidence: 99%

Paeonol Protects Against Myocardial Ischemia/Reperfusion-Induced Injury by Mediating Apoptosis and Autophagy Crosstalk

Tsai

Chen

et al. 2021

Front. Pharmacol.

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Many studies have shown that crosstalk exists between apoptosis and autophagy, despite differences in mechanisms between these processes. Paeonol, a major phenolic compound isolated from Moutan Cortex Radicis, the root bark of Paeonia × suffruticosa Andrews (Paeoniaceae), is widely used in traditional Chinese medicine as an antipyretic, analgesic and anti-inflammatory agent. In this study, we investigated the detailed molecular mechanisms of the crosstalk between apoptosis and autophagy underlying the cardioprotective effects of paeonol in rats subjected to myocardial ischemia/reperfusion (I/R) injury. Myocardial I/R injury was induced by occlusion of the left anterior descending coronary artery (LAD) for 1 h followed by 3 h of reperfusion. Paeonol was intravenously administered 15 min before LAD ligation. We found that paeonol significantly improved cardiac function after myocardial I/R injury and significantly decreased myocardial I/R-induced arrhythmia and mortality. Paeonol also significantly decreased myocardial infarction and plasma LDH activity and Troponin-I levels in carotid blood after I/R. Compared with vehicle treatment, paeonol significantly upregulated Bcl-2 protein expression and significantly downregulated the cleaved forms of caspase-8, caspase-9, caspase-3 and PARP protein expression in the I/R injured myocardium. Myocardial I/R-induced autophagy, including the increase of Beclin-1, p62, LC3-I, and LC3-II protein expression in the myocardium was significantly reversed by paeonol treatment. Paeonol also significantly increased the Bcl-2/Bax and Bcl-2/Beclin-1 ratios in the myocardium after I/R injury. The cardioprotective role of paeonol during I/R injury may be due to its mediation of crosstalk between apoptotic and autophagic signaling pathways, which inhibits apoptosis and autophagic cell death.

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“…Skin stimulation agents, including LPS, TNF-α, or DNCB, act as irritants to keratinocytes, and these stimulated keratinocytes, in turn, activate the MAPK, Akt, and NF-κB signaling pathways [ 36 ]. The p -p38 pathway is more responsive to oxidative stress than other MAPK signaling pathways (such as p-ERK and p-JNK) [ 37 ], and the p -p38 pathway is involved in the chronic phase of AD pathogenesis [ 38 ]. NF-κB is a transcription factor that facilitates allergic diseases, such as AD and asthma, by increasing the levels of inflammatory cytokines [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Immunomodulatory and Anti-inflammatory Effects of Asiatic Acid in a DNCB-Induced Atopic Dermatitis Animal Model

et al. 2021

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We examined the immunomodulatory and anti-inflammatory effects of asiatic acid (AA) in atopic dermatitis (AD). AA treatment (5–20 µg/mL) dose-dependently suppressed the tumor necrosis factor (TNF)-α level and interleukin (IL)-6 protein expression in interferon (IFN)-γ + TNF-α-treated HaCaT cells. The 2,4-dinitrocholrlbenzene (DNCB)-induced AD animal model was developed by administering two AA concentrations (30 and 75 mg/kg/d: AD + AA-L and AD + AA-H groups, respectively) for 18 days. Interestingly, AA treatment decreased AD skin lesions formation and affected other AD characteristics, such as increased ear thickness, lymph node and spleen size, dermal and epidermal thickness, collagen deposition, and mast cell infiltration in dorsal skin. In addition, in the DNCB-induced AD animal model, AA treatment downregulated the mRNA expression level of AD-related cytokines, such as Th1- (TNF-α and IL-1β and -12) and Th2 (IL-4, -5, -6, -13, and -31)-related cytokines as well as that of cyclooxygenase-2 and CXCL9. Moreover, in the AA treatment group, the protein level of inflammatory cytokines, including COX-2, IL-6, TNF-α, and IL-8, as well as the NF-κB and MAPK signaling pathways, were decreased. Overall, our study confirmed that AA administration inhibited AD skin lesion formation via enhancing immunomodulation and inhibiting inflammation. Thus, AA can be used as palliative medication for regulating AD symptoms.

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Effect and mechanism of asiatic acid on autophagy in myocardial ischemia‑reperfusion injury <em>in vivo</em> and <em>in vitro</em>

Cited by 18 publications

References 54 publications

Asiatic Acid Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting the ROS-Mediated Mitochondria-Dependent Apoptosis Pathway

Asiatic Acid Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting the ROS-Mediated Mitochondria-Dependent Apoptosis Pathway

Paeonol Protects Against Myocardial Ischemia/Reperfusion-Induced Injury by Mediating Apoptosis and Autophagy Crosstalk

Immunomodulatory and Anti-inflammatory Effects of Asiatic Acid in a DNCB-Induced Atopic Dermatitis Animal Model

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