Affiliations: [a] Department of Cardiology, Yancheng Traditional Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Yancheng, Jiangsu, China | [b] Laboratory of Morphology, Xuzhou Medical University, Xuzhou, Jiangsu, China | [c] Department of Integrated Traditional and Western Medicine, The Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China | [d] Department of Treating disease center, Changzhou Traditional Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Changzhou, Jiangsu, China
Correspondence:
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Corresponding author: Xiaolong Song, Department of Cardiology, Yancheng Traditional Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Yancheng, Jiangsu, China. E-mail: [email protected].
Abstract: BACKGROUND: Hypertension is a well-recognized risk factor for cardiovascular, which is also a critical factor in causing myocardial fibrosis (MF). OBJECTIVE: The study aimed to explore the effect of Atractylenolide II (ATL-II) on MF and oxidative stress in spontaneous hypertension rats (SHR). METHODS: The body weight of rats after injection of ATL-II was quantitatively analyzed. The left ventricular function of SHR was evaluated by Echocardiographic. HE staining, Masson trichrome staining, left ventricular mass index (LVMI) and immunofluorescence was applied to investigate the effects of ATL-II on MF. RT qPCR was used to detect the Collagen I, α-SMA, Fibronectin, and Vimentin mRNA expression levels in myocardial slices. The effect ATL-II on cardiomyocyte apoptosis was detected by TUNEL staining and western blot. An immunohistochemistry assay was conducted to detect α-SMA protein and TGF-β1 protein. The contents of H2O2, GSH-PX, SOD, and MDA were measured by colorimetry. RESULTS: ATL-II could dose-dependently improve the BW of SHRs (P< 0.05) and enhance myocardial function. Moreover, ATL-II effectively reduced cardiomyocyte apoptosis in SHRs. Alternatively, ATL-II could inhibit the Collagen I, α-SMA, Fibronectin, and Vimentin mRNA and protein expression levels in SHRs. ATL-II could ameliorate oxidative stress by improving the activities of SOD and GSH-PX and lowering the contents of H2O2 and MDA in ATL-II-treated SHRs, which reach about 80%. CONCLUSION: ATL-II could exert an inhibiting effect on MF and oxidative stress in SHRs. Hence, ATL-II may hold promise for the treatment of MF and oxidative stress in Spontaneous Hypertension.
