Citri reticulatae Pericarpium attenuates Ang II-induced pathological cardiac hypertrophy via upregulating peroxisome proliferator-activated receptors gamma.
Citri reticulatae Pericarpium attenuates Ang II-induced pathological cardiac hypertrophy via upregulating peroxisome proliferator-activated receptors gamma.
复制标题
柑橘皮通过上调过氧化物酶体增殖物激活受体 γ 减弱血管紧张素 II 诱导的病理性心脏肥大
DOI：
10.21037/atm-20-2118
复制
发表时间：
2020-09
影响因子：
--
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Ni G;Wang K;Zhou Y;Wu X;Wang J;Shang H;Wang L;Li X
背景：病理性心肌肥厚是包括心力衰竭在内的心血管疾病的主要危险因素。然而，可用于逆转适应不良过程和恢复心脏功能的药物治疗有限。陈皮已被用于临床治疗的中医方剂中。先前的研究表明，C反应蛋白及其成分对心血管系统有有益的影响。然而，C反应蛋白是否对病理性心肌肥厚有保护作用仍不清楚。方法用血管紧张素II(Ang II)诱导原代新生大鼠心肌细胞发生病理性肥大。免疫荧光染色和实时定量聚合酶链式反应(qRT-PCR)分别检测细胞大小和肥大基因标志物(ANP和BNP)的表达。对雄性C57BL/6小鼠进行血管紧张素转换酶II(Ang II，2.5 mg/kg/d，连续4周)诱导的心肌肥大实验。给予C-反应蛋白(0.5g/kg/d，连续4周)治疗，观察心肌肥厚(苏木精-伊红染色和定量逆转录聚合酶链式反应)、心肌纤维化(马森氏三色染色、定量逆转录聚合酶链式反应和免疫印迹)和心功能(超声心动图)。用免疫印迹法检测PPARγ和PGC-1α在NRCM和小鼠体内的蛋白水平。结果发现C反应蛋白可抑制血管紧张素Ⅱ诱导的病理性心肌肥厚，表现为改善心功能、减少肥大生长和减轻心肌纤维化。此外，我们还证明了PPARγ在NRCM和心脏中均被C反应蛋白上调。此外，PPARγ抑制剂可阻断C反应蛋白对血管紧张素Ⅱ诱导的病理性心肌肥厚的抑制作用。结论C反应蛋白通过激活PPARγ减轻血管紧张素Ⅱ诱导的病理性心肌肥厚。
Background Pathological cardiac hypertrophy is a major risk factor for cardiovascular diseases, including heart failure. However, limited pharmacological therapies are available for reversing the maladaptive process and restoring cardiac function. Citri reticulatae Pericarpium (CRP) has been used in traditional Chinese medicine prescriptions for clinical treatment. Previous studies have shown that CRP and its ingredients have beneficial effects on the cardiovascular system. However, whether CRP has a protective effect against pathological cardiac hypertrophy remains unknown. Methods Primary neonatal rat cardiomyocytes (NRCMs) were treated with angiotensin II (Ang II) to induce pathological hypertrophy in vitro. Immunofluorescent staining and quantitative real-time PCR (qRT-PCR) were used to determine the cell size and the expression of hypertrophic gene markers (Anp and Bnp), respectively. Male C57BL/6 mice were subjected to the investigation of cardiac hypertrophy induced by Ang II (2.5 mg/kg/d for 4 weeks). CRP (0.5 g/kg/d for 4 weeks) was administrated to treat mice with or without peroxisome proliferator-activated receptors gamma (PPARγ) inhibitor T0070907 (1 mg/kg/d for 4 weeks treatment) infused with Ang II. Cardiac hypertrophy (hematoxylin-eosin staining and qRT-PCR), fibrosis (Masson’s Trichrome staining, qRT-PCR, and western blot), and cardiac function (echocardiography) were examined in these mice. Western blot was used to determine the protein level of PPARγ and PGC-1α both in NRCMs and in mice. Results We found that CRP could prevent Ang II-induced pathological cardiac hypertrophy evidenced by improving cardiac function, decreasing hypertrophic growth and reducing cardiac fibrosis. Also, we demonstrated that PPARγ was upregulated by CRP both in NRCMs and in hearts. Moreover, PPARγ inhibitor could abolish the inhibitory effects of CRP on Ang II-induced pathological cardiac hypertrophy. Conclusions CRP attenuates Ang II-induced pathological cardiac hypertrophy by activating PPARγ.
登录
查看更多内容
胡椒碱通过 PPAR-gamma/AKT 途径减轻病理性心脏纤维化
影响因子：
11.1
作者：
Ma ZG;Yuan YP;Zhang X;Xu SC;Wang SS;Tang QZ
通讯作者：
Tang QZ
影响因子：
5.6
作者：
Sp N;Kang DY;Joung YH;Park JH;Kim WS;Lee HK;Song KD;Park YM;Yang YM
通讯作者：
Yang YM
CRM1 抑制剂可减轻心脏肥大并增加 NRVM 中 NT-PGC-1 α 的核分布
影响因子：
5.6
作者：
Liu, Zuheng;Tian, Haiping;Xu, Dingli
通讯作者：
Xu, Dingli
影响因子：
8
作者：
Kong, Ping;Christia, Panagiota;Frangogiannis, Nikolaos G.
通讯作者：
Frangogiannis, Nikolaos G.
miR-17-3p有助于运动诱导的心脏生长并预防心肌缺血再灌注损伤
影响因子：
12.4
作者：
Shi J;Bei Y;Kong X;Liu X;Lei Z;Xu T;Wang H;Xuan Q;Chen P;Xu J;Che L;Liu H;Zhong J;Sluijter JP;Li X;Rosenzweig A;Xiao J
通讯作者：
Xiao J