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The effect of curculigo orchioides (Xianmao) on kidney energy metabolism and the related mechanism in rats based on metabolomics. | LitMetric

AI Article Synopsis

Article Abstract

The Chinese materia medica Xianmao (XM) is widely used in Chinese clinics and the traditional Chinese medicine diets. Although XM is often used to study its kidney-yang effect, the research on its effect on kidney energy metabolism and its mechanism is still relatively lacking. In this study, rats were given different doses of XM water extract for 4 weeks. Biochemical method was used to detect the content of serum biochemical indexes of liver and kidney function and blood lipid indicators, and HE staining method was used to observe the histopathological of liver and kidney in rats. The kidney Na-K-ATPase, Ca-Mg-ATPase, SDH (succinate dehydrogenase) enzyme activity, and the content of ATP in rats were measured. Metabolomics technology was used to analyze the potential biomarkers related to the effects of XM on kidney energy metabolism, and then, the metabolic pathways were analyzed. RT-PCR was used to detect the expression of Ampk, Sirt1, Ppar-α, and Pgc-1α mRNA in kidney of rats. The results showed, compared with the blank control group, there was no significant effect on liver and kidney function in XMH, XMM, and XML groups. These significantly increased the kidney Na-K-ATPase, Ca-Mg-ATPase, SDH enzyme activity, and ATP content in XMH, XMM, and XML groups. Mitochondrial metabolic rate was inhibited in XMH group, but it was significantly increased in XMM and XML groups. The number of mitochondria was increased in XMH, XMM, and XML groups. Overall, these effects may be mediated by TCA cycle metabolism, butanoate metabolism, propanoate metabolism, alanine, aspartate, and glutamate metabolism, retinol metabolism, purine metabolism, pentose phosphate metabolism, aminoacyl-tRNA biosynthesis, valine, leucine, and isoleucine biosynthesis, and degradation metabolism pathways, as well as by increasing expression of upstream genes Ampk, Sirt1, Ppar-α, and Pgc-1α mRNA.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8565213PMC
http://dx.doi.org/10.1002/fsn3.2573DOI Listing

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