Andr significantly inhibited MAPKs activation in both mouse hearts and cardiomyocytes. In addition, cardiomyocytes treated with Andr showed a reduced hypertrophic response to angiotensin II. Andr treatment induced a strong reduction in the transcription of both hypertrophy (ANP, BNP, and β-MHC) and fibrosis related genes (collagen I, collagen III, CTGF, and TGFβ).
Our results showed that Andr administration for 7 weeks decreased cardiac dysfunction and attenuated cardiac hypertrophy and fibrosis in AB mice. Cardiac function was accessed by echocardiography and hemodynamic parameters.
Thus, mice were subjected to aortic banding (AB) with/without Andr administration (25 mg/kg/day, orally). Our aim was to evaluate the effects of Andr on cardiac hypertrophy and MAPKs activation. Andr has also been shown to inhibit inflammation and apoptosis, which are factors related to cardiac hypertrophy. Andrographolide (Andr), a botanical compound, has potent cardio-protective effects due to its ability to inhibit mitogen-activated protein kinases (MAPKs). Therefore, understanding the pathophysiological mechanisms involved in the remodeling process is crucial for the development of new therapeutic strategies.
3Hubei Key Laboratory of Cardiology, Wuhan, China.2Cardiovascular Research Institute, Wuhan University, Wuhan, China.1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
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