Indonesian herbal medicine prevents hypertension-induced left ventricular hypertrophy by diminishing NADPH oxidase-dependent oxidative stress
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Erna Sulistyowati1,2, Jong-Hau Hsu1,3,4, Yuan-Bin Cheng5, Fang-Rong Chang5,10, Ying-Fu Chen1,6,7 and Jwu-Lai Yeh1,8,9,10
1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
2Faculty of Medicine, Islamic University of Malang, Malang, East Java Province, Indonesia
3Department of Pediatrics, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
4Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
5Graduate Institute of Natural Products, College of Pharmacy, Kaohsiung, Taiwan
6Division of Cardiovascular Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
7Sin-Lau Christian Hospital, Tainan, Taiwan
8Department of Pharmacology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
9Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
10Department of Marine Biotechnology and Resources, National Sun Yat-Sen University, Kaohsiung, Taiwan
Jwu-Lai Yeh, email: firstname.lastname@example.org
Ying-Fu Chen, email: email@example.com
Keywords: Indonesian traditional medicine, hypertension, oxidative stress, NADPH oxidase
Received: August 03, 2017 Accepted: September 03, 2017 Published: September 30, 2017
Indonesian herbal medicine Centella asiatica, Justicia gendarussa and Imperata cylindrica decoction (CJID) are known to be efficacious for hypertension. Oxidative stress plays an important role in hypertension-induced left ventricular hypertrophy (H-LVH). This study evaluated whether CJID inhibit cardiac remodeling in spontaneously hypertensive rats (SHRs) through mechanism of oxidative stress-related cardiac-NADPH oxidase (NOXs) pathway: NOX1, NOX2 and NOX4. Forty-weeks-old SHRs and normotensive-WKY rats, were both randomly divided into 2 groups: CJID and control. All rats were treated for 5 weeks. Systolic blood pressure (SBP) and heart rate (HR) were measured. LV morphology, function and performance were assessed by histological staining and echocardiography. Serum and cardiac superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were assessed. Cardiac superoxide and hydrogen peroxide (H2O2) productions, protein expressions of SOD2, SOD3, NOX1, NOX2 and NOX4 were also determined. We found that SBP and HR were significantly decreased in SHRs-treated group. Echocardiography showed that CJID significantly improved LV morphometry and function. CJID decreased MDA level, but increased SOD activity. Cardiac superoxide and H2O2 generation were decreased in SHRs-treated group. CJID caused cardiac SODs expressions to be increased but NOXs expressions to be suppressed. In conclusion, CJID prevents H-LVH by reducing reactive oxygen species production via the NOXs-dependent pathway.
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