The Effect of Pravastatin on Expression of ENOS, ET-1, Nephrine, VEGF, TNF-Α, And IL-10 on Tissue Kidney Rat Model of Preeclampsia

Abstract

Background: Preeclampsia is known as a disease originating from placental and maternal dysfunction. Placental dysfunction can cause cellular, molecular, immunological, and vascular changes. In patients with preeclampsia, impaired renal function is often found even before clinical manifestations of proteinuria are detected. Preeclampsia is associated with glomerular lesions that are characteristically described as glomerular capillary endotheliosis. Pravastatin has a protective role at the uteroplacental and vascular endothelial cell interface, and has pleiotropic effects that may protect against preeclampsia such as endothelial protection, antioxidant properties, anti-inflammatory effects, anti-thrombotic effects, and possibly pro-angiogenic effects.

Objective: To determine the effect of pravastatin administration on kidney repair in preeclampsia rat models.

Methods: Post-test group-only experimental study using kidney tissue from the preeclampsia Rattus norvegicus model (exposed to L-NAME) and given pravastatin at various doses (2 mg, 4 mg, and 8 mg).

Results: The results of the One Way Anova test on the expression of eNOS, ET-1, nephrin, VEGF, TNFα, and IL10 in the five observation groups had a p-value <α (0.000; 0.000; 0.000; 0.001; 0.037; 0.000). The correlation test between eNOS, Nephrine and IL-10 expression with pravastatin dose was 0,712; 0.748; 0.593 (a positive correlation). p-value between VEGF expression with pravastatin dose is 0,376 (no correlation). The correlation between ET-1 and TNF-α expression with pravastatin dose was -0,928; -0,424 (a negative correlation). 

Conclusion: Pravastatin can decrease the expression of ET-1, and TNF-α increase the expression of nephrine, VEGF, eNOS, IL-10. These effect correlate to the increasing pravastatin  dosage