The following is the summary of “Rosiglitazone attenuates hypoxia-induced renal cell apoptosis by inhibiting NF-κB signaling pathway in a PPARγ-dependent manner” published in the November 2022 issue of Renal failure by Wei, et al.

Recently, it has been discovered that hypoxic renal illness is intimately linked to peroxisome proliferator-activated receptors (PPAR). This research set out to learn more about how rosiglitazone might affect mitochondrial apoptosis in renal tissue. A total of 24 male Sprague-Dawley rats were split into 3 groups (n=8 in each): normal control, hypoxic damage (identical volume of 0.9% saline), and PPAR agonist (Rosiglitazone, 10 mg/kg d, intraperitoneally). 

The hypoxia damage and PPARγ agonist groups spent 7 days at a simulated altitude of 7,000 m in a hypoxia chamber. After 7 days, samples of blood and kidneys were taken. Expression levels of PPAR, (NF-κB), B-cell lymphoma-2 (Bcl-2), and Bax were measured using quantitative real-time polymerase chain reaction and Western blotting. Massive renal tubular epithelial cell degeneration and detachment, as well as renal tubular dilatation were observed in the hypoxia group compared to the control group. 

Increased NF-κB protein expression, decreased Bcl-2 protein and mRNA expression, and increased Bax protein and mRNA expression were all statistically significant at the (P<.05) level. The PPAR agonist group experienced much less severe renal injury than the hypoxic injury group. Inhibition of NF-κB signaling pathway activation in a PPARγ-dependent manner, together with increases in Bcl-2 and decreases in Bax expression, are proposed mechanisms by which rosiglitazone protects against hypoxia-induced kidney impairment.