Study on the Mechanism of the Buqi Tongqiao Formula in Regulating the PI3K/AKT/mTOR Pathway to Intervene in IgA Nephropathy in Rats
DOI:
https://doi.org/10.54097/4kk71643Keywords:
IgA Nephropathy, Buqi Tongqiao Formula, PI3K/AKT/mTOR, Renal InjuryAbstract
Objective: To explore the molecular mechanism by which Buqi Tongqiao Formula (BQTQF) improves renal injury in rats with IgA nephropathy (IgAN) by regulating the PI3K/AKT/mTOR pathway. Methods: The IgAN rat model was established by intragastric administration of BSA, intraperitoneal injection of CCl₄, and combined intravenous injection of LPS. Thirty rats were randomly divided into the blank group, model group, and BQTQF group. After successful model establishment, the rats were administered continuously for 8 weeks, once a day. Renal function was evaluated by determining 24-hour urinary protein, Scr, and BUN levels. Pathological damage of renal tissue in IgAN rats was observed by HE staining. RT-qPCR and Western blot were used to detect the mRNA and protein expression levels of PI3K, AKT, and mTOR in renal tissue of IgAN rats. Results: Compared with the blank group, the levels of 24hUTP, Scr, and BUN in the model group were significantly increased (P<0.01), renal pathological damage was aggravated, and the mRNA transcription levels and protein expression of PI3K, AKT, and mTOR in renal tissue were elevated. After intervention with BQTQF, the renal function of IgAN rats was significantly improved, histopathological damage was alleviated, and the mRNA transcription levels and phosphorylated protein expression of PI3K, AKT, and mTOR were reduced. Conclusion: BQTQF alleviates renal pathological damage and improves renal function in IgAN rats by regulating the PI3K/AKT/mTOR signaling pathway.
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