Department of Urology Surgery, Hospital of Chengdu University of Traditional Chinese Medicine, No. 39, Twelve Bridges Road, Jinniu District, Chengdu, 610072, Sichuan Province, China.
Department of Nursing, Hospital of Chengdu University of Traditional Chinese Medicine, No. 39, Twelve Bridges Road, Jinniu District, Chengdu, 610072, Sichuan Province, China.
Int Urol Nephrol. 2023 Oct;55(10):2421-2429. doi: 10.1007/s11255-023-03641-x. Epub 2023 Jun 27.
Sanjin Paishi Decoction (SJPSD) has positive effects on stone prevention; however, there is a lack of convincing evidence in the prevention of calcium oxalate stones. This study aimed investigates the effect of SJPSD on calcium oxalate stones and to explore its mechanism.
The rat model of calcium oxalate stones was established and rats were treated with different doses of SJPSD. The pathological damage of kidney tissues was observed by HE staining, the deposition of calcium oxalate crystals in kidney tissues was examined by Von Kossa staining, and the levels of creatinine (CREA), urea (UREA), calcium (Ca), phosphorus (P), and magnesium (Mg) in serum were analyzed biochemically, the levels of IL-1β, IL-6, and TNF-α in serum were measured by ELISA, and the protein expression of Raf1, MEK1, p-MEK1, ERK1/2, p-ERK1/2, and Cleaved caspase-3 in kidney tissues was analyzed by Western blot. Moreover, the changes in gut microbiota were analyzed by 16S rRNA sequencing.
SJPSD attenuated the pathological damage of renal tissues, reduced the levels of CREA, UREA, Ca, P, and Mg, and inhibited the expression of Raf1, p-MEK1, p-ERK1/2, and Cleaved caspase-3 in renal tissues (P < 0.05). SJPSD treatment affected the composition of intestinal microbiota in rats with calcium oxalate stones.
The mechanism of SJPSD inhibition of calcium oxalate stone injury in rats may be related to the inhibition of the MAPK signaling pathway and regulation of gut microbiota imbalance.
三金排石汤(SJPSD)对结石预防有积极作用,但在预防草酸钙结石方面缺乏令人信服的证据。本研究旨在探讨 SJPSD 对草酸钙结石的作用及其机制。
建立大鼠草酸钙结石模型,用不同剂量 SJPSD 处理大鼠。通过 HE 染色观察肾组织的病理损伤,通过 Von Kossa 染色观察肾组织中草酸钙晶体的沉积,用生化方法分析血清中肌酐(CREA)、尿素(UREA)、钙(Ca)、磷(P)和镁(Mg)的水平,用 ELISA 法测定血清中白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的水平,用 Western blot 法分析肾组织中 Raf1、MEK1、p-MEK1、ERK1/2、p-ERK1/2 和 Cleaved caspase-3 的蛋白表达。此外,还通过 16S rRNA 测序分析肠道微生物群的变化。
SJPSD 减轻了肾组织的病理损伤,降低了 CREA、UREA、Ca、P 和 Mg 的水平,并抑制了肾组织中 Raf1、p-MEK1、p-ERK1/2 和 Cleaved caspase-3 的表达(P<0.05)。SJPSD 治疗影响了草酸钙结石大鼠肠道微生物群的组成。
SJPSD 抑制大鼠草酸钙结石损伤的机制可能与抑制 MAPK 信号通路和调节肠道微生物群失衡有关。