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Pioglitazone Ameliorates Hypertension Induced Cardiac Hypertrophy and Down Regulates Cardiac Hypoxia Inducible Factor-l α in Rats

Pioglitazone Ameliorates Hypertension Induced Cardiac Hypertrophy and Down Regulates Cardiac Hypoxia Inducible Factor-l α in Rats

You-Ming Teng, Wen-Zhou Liu and Li Yang*

Department of Cardiology, Guangxi Medical University, Nanning city, Guangxi Province, 530028, China

 
* Corresponding author: [email protected]

ABSTRACT

It is known that cardiac hypertrophy induced by hypertension always goes with abnormal myocardial glucolipid metabolism. However, whether or not pioglitazone may alleviate the cardiac hypertrophy and reverse abnormal myocardial glucolipid metabolism is still unknown. We conducted this experiment to explore the influence of pioglitazone on cardiac hypertrophy in rats. Rats with cardiac hypertrophy induced by renovascular hypertension were given a gavage of pioglitazone 5–10 mg/kg for 4 weeks. Our crew determined systolic blood pressure (SBP) and diastolic blood pressure (DBP). Heart mass index (HMI), left ventricular mass index (LVMI), myocardial cell diameter (MCD) and surface area (SA) were further estimated. We members determined FFA and Ang II levels. HE and Masson staining were estimated histopathological changes. The protein and mRNA expression of PPAR-α, CPT-1 as well as PDK-4 were measured by western blot and qRT-PCR. The results showed that pioglitazone could reduced SBP, DBP, MCD, SA, HMI, LVMI as well as myocardial fibrosis and FFA and Ang II levels in serum. Moreover, pioglitazone inhibited the expression of HIF-1α protein and simultaneously enhanced the expressions of PPAR-α, CPT-1 as well as PDK-4 mRNA and proteins. So we infer that pioglitazone could improve hypertension-induced cardiac hypertrophy and redress abnormal myocardial glucolipid metabolism in rats by down-regulating the protein expression of myocardial HIF-1α and increasing the protein expressions of myocardial PPARα, CPT-1 and PDK-4.

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Pakistan Journal of Zoology

October

Pakistan J. Zool., Vol. 56, Iss. 5, pp. 2001-2500

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