背景:三金排石汤(SJPSD)对预防结石具有积极作用;然而,在预防草酸钙结石方面缺乏令人信服的证据。本研究旨在研究SJPSD对草酸钙结石的影响并探讨其机制。
方法:建立大鼠草酸钙结石模型,用不同剂量的SJPSD治疗大鼠。HE染色观察肾组织病理损伤,通过VonKossa染色检查了草酸钙晶体在肾脏组织中的沉积,和肌酐水平(CREA),尿素(UREA),钙(Ca),磷(P),血清中的镁(Mg)进行生化分析,IL-1β水平,ELISA法测定血清中IL-6和TNF-α,通过Westernblot分析肾组织中Raf1,MEK1,p-MEK1,ERK1/2,p-ERK1/2和Cleavedcaspase-3的蛋白表达。此外,通过16SrRNA测序分析肠道菌群的变化。
结果:SJPSD减轻了肾组织的病理损伤,降低了CREA的水平,尿素,Ca,P,Mg,并抑制肾组织中Raf1、p-MEK1、p-ERK1/2和Cleavedcaspase-3的表达(P<0.05)。SJPSD治疗影响草酸钙结石大鼠肠道菌群的组成。
结论:SJPSD抑制草酸钙结石大鼠损伤的机制可能与抑制MAPK信号通路和调节肠道菌群失衡有关。
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.