Abstract

Context: The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear.

Objective: To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy.

Materials and methods: Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting.

Results: DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively).

Discussion and conclusions: DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy.

摘要

背景：铁皮石end墙壁的药理作用。前林德尔。（兰花科）心脏肥大仍不清楚。

目的：为了评估是否D.石斛水性提取物（DCAE）可以衰减实验性心肌肥厚。

材料与方法：皮下注射异丙肾上腺素（2 mg / kg），每天一次，持续10天，从而诱发SD大鼠心脏肥大。每天用DCAE（0.13和0.78 g / kg）灌胃大鼠，持续一个月。在治疗结束时，测量左心室收缩压（LVSP），心体重比（HW / BW），左心室/胫骨长度（LV / TL），心房利钠肽（ANP），脑利钠肽（BNP）水平，苏木精-伊红染色和Masson三色染色。在培养的H9c2细胞中，在异丙肾上腺素（10μM）刺激前2小时加入DCAE（2 mg / mL）和U0126（10μM）。鬼笔环肽染色用于评估细胞肥大。通过qRT-PCR测量ANP和BNP的mRNA表达。通过免疫印迹测定p-ERK的表达。

结果： DCAE治疗显着降低了以下体内指标：（1）LVSP（16％）；（2）硬件/体重（13％）; （3）LV / TL（6％）；（4）ANP（39％）；（5）法国巴黎银行（32％）。在培养的H9c2细胞中，鬼笔环肽染色显示DCAE可以缓解细胞肥大（减少53％）。此外，免疫印迹显示DCAE可以在体内和体外显着抑制p-ERK蛋白表达（分别降低39％和27％）。

讨论与结论： DCAE可通过ERK信号传导途径预防心脏肥大，并具有治疗心脏肥大的潜力。