Rahman, Mohammad Saifur
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EVALUATION OF SST-2 ROLE IN LVH REGRESSION OBTAINED IN HYPERTENSIVE MICE MODELS AFTER BLOCKING RENIN-ANGIOTENSIN SYSTEM Yusetyani, Lilik; Rofida, Siti; Lestari, Dian Yuliartha; Kurniawan, Wawan; Hijriani, Nursela; Saputra, Ilham Niawan; Soeharto, Setyawati; Rahman, Mohammad Saifur
Journal of Tropical Life Science Vol 9, No 1 (2019)
Publisher : Journal of Tropical Life Science

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Abstract

Soluble ST2, is a protein which acts as a decoy receptor for interleukin-33, and served as biomarker associated with left ventricular hypertrophy (LVH).  Few data exist in evaluating the effects of anti-hypertensive agents on the role-played form ST2 on regression of LVH. This study was designed to compare the effects of captopril and valsartan on blood pressures, plasma renin and soluble ST2 levels and regression of LVH in hypertensive mice models. Twenty-four male mice (Mus musculus L), were divided into four groups, namely aquadest/control, L-NAME, L-NAME + captopril and L-NAME + valsartan groups respectively. Mice blood pressures were measured on day 14th after induction with L-NAME extract 1.75 mg/25 g BW/day (pretreatment) and day 14th post treatment. Levels of plasma renin, sST2, and ventricular wall thicknesses reflecting LVHs, were measured on day 14th post treatment. Administration of L-NAME within 14 days resulted in making mice models to be hypertensive paralleled by an increase of Ventricular wall thickness. Treatment with captopril and valsartan lowered the blood pressures to normal level within the next 14 days. Valsartan and captopril treatment induced a significant decrease of plasma renin level. Valsartan, but not for captopril treatment prevented wall thickness increase (p < 0.05), while plasma sST2 was not able to mirroring this effect. Captopril and valsartan had similar effect in lowering plasma renin level and   blood pressure, but sST2 seems to be not involved in LVH regression obtained in hypertensive mice models after blocking renin-angiotensin system.
Prominently Increased of Mannose Binding Lectin (MBL) and Myeloperoxidase (MPO) Levels in Severe Valve Regurgitation and Heart Failure of Rheumatic Heart Disease Putri, Rachmania; Suwarniaty, Renny; Fitri, Loeki Enggar; Nugroho, Susanto; Rahman, Mohammad Saifur
Journal of Tropical Life Science Vol 7, No 2 (2017)
Publisher : Journal of Tropical Life Science

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.11594/jtls.07.02.04

Abstract

Rheumatic heart disease (RHD) is mediated by an abnormal immunological response following a Streptococcus pyogenes infection that induces a disturbance of oxidants and antioxidants balances. Mannose-binding lectin (MBL) binds to N-acetylglucosamine, a molecule present on the Streptococcus cell wall and human heart valves. There is a disturbance of oxidant and antioxidant balance in rheumatic disease. Myeloperoxidase (MPO) is a marker of oxidative stress and inflammation. This study was aimed to determine the correlation of MBL and MPO levels and severity of valvular regurgitation and heart failure (HF) in RHD patients. A case-control study was conduct using human peripheral blood samples from 32 children aged 6 to 14 years old. The subjects were divided into two groups: 16 RHD patients included in the case group and 16 healthy children as a control group. The level of MBL and MPO was investigated using ELISA method. There were significant differences on MBL and MPO level between patient and control group. The level of MBL and MPO were significantly increased in RHD group, especially on severe valvular regurgitation. There was a strong correlation between MBL and MPO levels and the severity of valvular regurgitation (r = 0.94 and r = 0.88). The least significant diff-erence (LSD) analysis showed that significant difference occurs in the severe heart failure group. Our research revealed that the MBL and MPO levels in pediatric RHD patients were significantly higher than in healthy children. The MBL and MPO levels were significantly correlated with the severity of valvular regurgitation and heart failure.