ABSTRACT
Background The customary puerperal practice of Natron consumption has been identified as one of the predisposing factors in the etiology of peripartum cardiomyopathy (PPCM). This study was designed to investigate the effect of Natron in postpartum Wistar albino rats. Methods A total of 30 postpartum Wistar rats were exposed to different doses (50 mg/kg, 100 mg/kg, 200 mg/kg and 300 mg/kg) of Natron for 28 days. After the treatment, we carried out biochemical analyses and histological evaluations of kidney, liver and heart. Results The study revealed that the exposure of postpartum rats to 100 mg/kg of Natron and above significantly (p < 0.05) increase the cardiac markers; myoglobin, creatine kinase-MB, troponin I and T as compared with control. The result of liver function indicated no significant difference in alanine aminotransferase, aspartate aminotransferase, gamma-glutamyltransferase, albumin and total protein of the Natron treated groups as compared with control. However, at higher doses, the levels of total protein, globulin and alkaline phosphatase activity were significantly increased in comparison to the control. There was no significant difference in the kidney function markers of the treatment groups as compared with control. Histological examinations revealed no changes in the kidney of the treated groups. Mild portal triaditis was observed in the liver of the treated rats. The heart of the rats administered ≥100 mg/kg of Natron showed myocyte hypertrophy. Conclusion The study demonstrated that the administration of Natron for 28 days caused changes in the heart of postpartum rats and thus may contribute to the pathogenesis of PPCM.
ABSTRACT
Aim To study the effect of ginsenoside Rg1(Rg1)on cardio myocyte hypertrophy induced by prostaglandin F2?(PGF2?),and to probe primarily into its mechanism.Methods The cultured neonatal rat cardiomyocyte hypertrophic response and the antihypertrophic effects of Rg1 were observed by measuring the cell diameter,protein content and the expression of atrial natriuretic factor(ANF) mRNA,which was assayed by real-time PCR.For mechanism studies,the intracellular free calcium concentration(i) in cultured cardiomyocytes was measured by using Fura-2/AM as a fluorescent indicator,nitric oxide(NO) metabolite level in the culture medium was tested by using Nitric Oxide Synthase Detection Kit.Results PGF2? 0.1 ?mol?L-1 caused the increases in the cardiomyocyte cell diameter,protein content and the expression of ANF mRNA.It could increase the i in cultured cardiomyocytes.Rg1 15.6、31.2、62.4 ?mol?L-1 could concentration-dependently inhibit the cardiomyocyte hypertrophy induced by PGF2?,and the cell diameter of cardiomyocyte treated by PGF2? was decreased by 18.4%、32.7%、43.8%(P