Rosiglitazone attenuates hypoxia-induced renal cell apoptosis by inhibiting NF-?B signaling pathway in a PPAR?-dependent manner

Background: In recent years, peroxisome proliferator-activated receptor gamma (PPAR gamma) has been found to be closely associated with hypoxia renal disease. The aim of this study was to investigate the relationship between rosiglitazone and mitochondrial apoptosis in renal tissue and its associated mechanisms. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into three groups (n = 8 in each): normal control group, hypoxia injury group (equal volume of 0.9% saline), and PPAR gamma agonist group (Rosiglitazone, 10 mg/kg.d, intraperitoneally). The hypoxia injury group and PPAR gamma agonist group were placed in a hypoxia chamber and the simulated altitude was set at 7,000 m for 7 days. Blood and kidney samples were collected after 7 days. The quantitative real-time polymerase chain reaction and Western blot methods were used to determine the expression of PPAR gamma, nuclear factor kappa-B (NF-kappa B), B-cell lymphoma-2 (Bcl-2), and Bax. Results: The results showed that compared with the normal control group, the renal tissue of rats after hypoxia was severely damaged, as shown by massive renal tubular epithelial cell degeneration and detachment, and renal tubular dilation. The NF-kappa B protein expression significantly increased, the Bcl-2 protein and mRNA expression significantly decreased, and Bax protein and mRNA expression significantly increased (p < .05 for all). Renal injury was much less severe in the PPAR gamma agonist group compared to the hypoxia injury group. Conclusions: Rosiglitazone can alleviate hypoxia renal injury, with the possible mechanism involving attenuation of apoptosis by inhibiting the activation of the NF-kappa B signaling pathway in a PPAR gamma-dependent manner and increasing Bcl-2 and decreasing Bax expression.

Automated summary

The study found that rosiglitazone can alleviate hypoxia renal injury by inhibiting the activation of the NF-κB signaling pathway, increasing Bcl-2 expression, and decreasing Bax expression. These findings are of great significance for a deeper understanding of the pathophysiology of kidney diseases and exploring new therapeutic approaches.