Exploring The Mechanism Of Action Of Cistanche Total Glycosides On Inflammatory Bowel Disease Based On Network Pharmacology And Animal Experiments Ⅳ

4 Discussion

IBD can cause chronic inflammation and ulcers of the intestinal mucosa, which cannot be completely cured by modern Western medicine and seriously affects the patient's quality of life [23-25]. Traditional Chinese medicine believes that adjusting diet can balance yin and yang in the body and help relieve intestinal inflammation [26]. Traditional Chinese medicine dietary therapy can play a positive role in the auxiliary treatment of inflammatory bowel disease. Cistanche deserticola can be used as a traditional health food raw material to assist in the treatment of inflammatory bowel disease.

Network pharmacology analysis showed that the total glycoside components of Cistanche deserticola have 254 targets that have a protective effect on IBD. GO enrichment results show that Cistanche deserticola total glycosides' intervention in IBD may be related to signal transduction, protein phosphorylation, negative regulation of apoptosis process, proteolysis, innate immune response, positive regulation of cell proliferation, cell differentiation, positive regulation of DNA template transcription, protein Binding, ATP binding, metal ion binding, zinc ion binding, protein serine/threonine/tyrosine kinase activity, enzyme binding and other biological processes and molecular functions. Active ingredient-target-pathway network analysis shows that the active ingredient of Cistanche deserticola may regulate cancer pathways, mTOR pathway, TGF-β pathway, JAK-STAT pathway, AMPK pathway, etc., thereby affecting cell signaling, proliferation, differentiation, apoptosis, etc.

According to the network pharmacology analysis results, the DSS-induced IBD mouse model was selected to simulate similar clinical symptoms of IBD patients to verify the analysis results. Existing studies indicate that TGF-β acts throughout

It plays a central role in the formation and occurrence of IBD. The large expression of TGF-β1 will lead to epithelial damage and abnormal repair of the colon, myofibroblast proliferation and subbasal membrane fibrosis, ultimately leading to the occurrence of IBD [27]. As an important protein substance, mTOR is a central regulator of cell growth and proliferation [28-29]. mTOR is involved in regulating many important cellular processes, including translation, transcription, and autophagy. Among them, the AMPK/mTOR signaling pathway can jointly mediate cell

Intracellular anabolic and catabolic processes [30-31]. In addition, the AMPK/mTOR pathway has also been confirmed to be an important pathway in regulating IBD disease [32]. mTOR is an important downstream signaling molecule of AMPK, which plays a negative regulatory role in the regulation of autophagy. TGF-β1 can also inhibit autophagy by regulating the expression level of mTOR-related signaling pathways, and can indirectly affect cells by mediating the SMADS signaling pathway. to the regulatory effect [31, 33]. This experiment focused on verifying mTOR and TGF-β

Expression of two signaling pathway genes. The results show that Cistanche deserticola total glycosides can effectively alleviate the weight loss and fecal bleeding of sick mice, reduce the DAI score, and inhibit the expression of mTOR and TGF-β signaling pathways in the spleen. Functional annotation analysis of PICRUSt2 gene by 16S rDNA amplicon sequencing of mouse feces. The results showed that the expression of COG1132, COG0745, COG1131, COG1961, COG0438, COG0534, COG0642, COG1595, COG0463, COG4974, COG2207, COG1136, and COG1309 functional genes was abnormally increased in the diseased mice. After intervention with Cistanche deserticola total glycosides

The expression of 13 genes returned to normal, while COG1028 and COG0451 genes were highly expressed. It is speculated that Cistanche deserticola total glycosides may regulate lipid metabolism, glucose metabolism and related defense signaling in mice.

signal transduction and other mechanistic processes to alleviate damage in IBD mice. The above experimental results are basically the same as those of network pharmacology analysis.

In summary, Cistanche deserticola total glycosides treat inflammatory bowel disease through multi-component, multi-target, and multi-pathway synergy. Its targets should be related to IL2, mTOR, TGF-β, JAK-STAT, NF-κB, etc. At the same time, experimental results show that Cistanche deserticola total glycosides may treat inflammatory diseases mainly by inhibiting the expression of TGF-β and mTOR signaling pathways. Enteropathy. This experiment provides a new method to elucidate the clinical application of Cistanche deserticola in the treatment of IBD. However, its specific mechanism and material basis require more in-depth research.

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