16S amplification sequencing of gut microbiota in SLE mouse model treated with Qihuang Jianpi Zishen decoction
Female MRL/lpr mice were randomly assigned to either the JPZS or vector group, while C57BL/6 mice served as the healthy control group. Renal outcomes, serum autoimmune and immune inflammatory indices were evaluated together with 16S rRNA sequencing of fecal microbiota, untargeted serum metabolomics, and renal transcriptomics, followed by comprehensive network analysis and targeted validation of glycolytic pathways. JPZS significantly reduced proteinuria, elevated serum creatinine, glomerular IgG deposition, and histopathological damage in MRL/lpr mice, and partially normalized circulating cytokines. JPZS reshaped lupus related intestinal dysbiosis, significantly enriched Akkermansia, and restored microbial pathways related to carbohydrate metabolism. Consistently, JPZS reshaped serum metabolites involved in amino acid and central carbon metabolism, and inhibited renal glycolytic gene features centered around hexokinase 3 (HK3). Targeted detection confirmed that after JPZS treatment, renal lactate levels decreased, lactate/pyruvate ratio decreased, and HK3 and Ldhal6b were down regulated. These findings suggest that JPZS improves lupus nephritis at least partially by enriching Akkermansia and inhibiting HK3 driven glycolysis in the kidneys, highlighting a metabolic mechanism that links traditional formulations with the gut kidney axis.