Citri Reticulatae Pericarpium protects against isoproterenol-induced chronic heart failure via activation of PPARγ.
Citri Reticulatae Pericarpium protects against isoproterenol-induced chronic heart failure via activation of PPARγ.
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Citri Reticulatae Pericarpium 通过激活 PPARγ 预防异丙肾上腺素诱导的慢性心力衰竭
DOI：
10.21037/atm-20-2200
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发表时间：
2020-11
影响因子：
--
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Cheng H;Wu X;Ni G;Wang S;Peng W;Zhang H;Gao J;Li X
背景 积累的临床试验和动物研究表明，七里强心（QLQX）是一种含有 11 种草药提取物的中药配方，对慢性心力衰竭（HF）具有有益作用。陈皮（CRP）是中药方中的一种草药，在中国已广泛用于治疗消化系统疾病、呼吸系统疾病和心血管疾病（CVD）。然而，CRP的心脏保护作用和机制尚不清楚。方法在异丙肾上腺素（ISO）诱导的慢性心力衰竭小鼠模型和用异丙肾上腺素处理的新生大鼠心室心肌细胞（NRVM）中研究CRP的作用。超声心动图用于确定心脏功能。使用苏木精-伊红（HE）染色和α-肌动蛋白免疫荧光染色来测量心肌细胞大小。通过马森三色染色评估心脏纤维化。通过实时定量PCR（qRT-PCR）测定心钠素多肽（ANP）和脑钠素多肽（BNP）的表达。 Western blot检测过氧化物酶体增殖物激活受体γ（PPARγ）、PPARγ辅激活因子1α（PGC-1α）、纤维化相关蛋白和凋亡相关蛋白的表达。结果我们发现CRP可以显着减轻ISO引起的心功能障碍，抑制心肌病理性肥厚，减轻心肌纤维化和细胞凋亡。从机制上讲，CRP 治疗可以逆转 ISO 注射小鼠心脏和 ISO 处理的 NRVM 中 PPARγ 和 PGC-1α 的下调。 CRP 对 ISO 诱发的心力衰竭的有益作用被 PPARγ 抑制剂 (T0070907) 消除，表明 CRP 介导的 PPARγ 上调对于 CRP 对 ISO 诱发的心功能障碍的预防作用至关重要。结论 总之，我们的研究表明，CRP 通过 PPARγ 激活减弱 ISO 诱导的心脏重塑，这代表了 CRP 在预防慢性心力衰竭方面的新应用。
Background Accumulated clinical trials and animal studies showed that Qiliqiangxin (QLQX), a traditional Chinese medicine formula containing extracts of 11 herbs, exerts beneficial effects on chronic heart failure (HF). Citri Reticulatae Pericarpium (CRP), one herbal medicine in QLQX, has been widely used in treatment against digestive, respiratory and cardiovascular diseases (CVDs) in China. However, the cardiac protective effects and mechanisms of CRP are still unclear. Methods The effects of CRP were investigated in isoproterenol (ISO)-induced chronic HF mice model and neonatal rat ventricular cardiomyocytes (NRVMs) treated with ISO. Echocardiography was used to determine cardiac function. Hematoxylin-eosin (HE) staining and α-actinin immunofluorescent staining were used to measure cardiomyocyte size. Cardiac fibrosis was evaluated by Masson’s trichrome staining. The expression of atrial natriuretic polypeptide (ANP) and brain natriuretic polypeptide (BNP) were determined by quantitative real time PCR (qRT-PCR). Western blot was applied to examine the expression of peroxisome proliferator-activated receptor gamma (PPARγ), PPARγ coactivator-1α (PGC-1α), fibrosis-related and apoptosis-related proteins. Results We found that CRP could significantly attenuate ISO-induced cardiac dysfunction, inhibit cardiac pathological hypertrophy and alleviate myocardial fibrosis and apoptosis. Mechanistically, the downregulation of PPARγ and PGC-1α in ISO-injected mice hearts and ISO-treated NRVMs could be reversed by CRP treatment. The beneficial effects of CRP against ISO-induced HF were abolished by PPARγ inhibitor (T0070907), suggesting that CRP-mediated PPARγ upregulation was essential for the preventive effect of CRP on ISO-induced cardiac dysfunction. Conclusions In conclusion, our study demonstrated that CRP attenuates ISO-induced cardiac remodeling via PPARγ activation, which represents a new application for CRP in the prevention of chronic HF.
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影响因子：
4.6
作者：
Piek A;de Boer RA;Silljé HH
通讯作者：
Silljé HH
DOI：
10.1016/j.bbamcr.2010.09.019
发表时间：
2011-07
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
Scarpulla RC
通讯作者：
Scarpulla RC
影响因子：
3.6
作者：
Bhargava, Poorva;Verma, Vipin Kumar;Arya, Dharamvir Singh
通讯作者：
Arya, Dharamvir Singh
影响因子：
2.1
作者：
Hohimer, AR;Davis, LE;Hatton, DC
通讯作者：
Hatton, DC
影响因子：
3.2
作者：
Branco, Ana F.;Moreira, Ana C.;Oliveira, Paulo J.
通讯作者：
Oliveira, Paulo J.