Phytomedicine : international journal of phytotherapy and phytopharmacology · 2024
Paeoniae radix alba improved intestinal mucosal microcirculation disturbance by regulating lncRNA MALAT1/HIF-1α pathway in the treatment of ulcerative colitis.
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Gu Yaru, Dong Zhikuo, Gu Ying, Gao Ya, Li Dantong, Zhang Yixin, Zhang Xiaoying
Аннотация
BACKGROUND: Microcirculatory problems in the intestinal mucosa are the primary cause of ulcerative colitis (UC). Although UC is commonly treated with paeoniae radix alba (PRA), its exact mechanism of action is unclear.
PURPOSE: To examine how PRA affects UC induced by dextran sulfate sodium (DSS) and the mechanism of its effects.
METHODS: The primary active components of PRA were identified using high-performance liquid chromatography (HPLC), and network pharmacology techniques were used to predict the possible targets of action and signaling pathways in treatment for UC. A model of UC was established in vivo using rats, and a PRA intervention was performed. The amounts of cytokines in the colonic tissues and serum were measured using enzyme-linked immunosorbent assay (ELISA). The permeability of the intestinal mucosa was measured using a fluorescein isothiocyanate (FITC)-dextran assay and western blot. A PeriCam PSI system was used to view the microcirculation of the intestinal mucosa, and immunohistochemistry and immunofluorescence stains were used to detect angiogenesis. An electron microscope was used to observe the damage to the endothelium of the colon. Western blot and immunohistochemistry analyses were used to evaluate the protein expression of hypoxia-inducible factor-1 alpha (HIF-1α) in colon tissues, and qRT-PCR was used to assess the lncRNA expression of MALAT1.
RESULTS: HPLC identified 10 main active components of PRA, and the network pharmacology results showed that the treatment of UC with PRA was associated with the HIF-1 signaling pathway. The results of animal experiments revealed that PRA significantly improved the pathological damage to the colon and the microcirculatory issues in the intestinal mucosa. PRA also inhibited colonic endothelial cell damage and angiogenesis, which may be related to the inhibition of the increased expression of lncRNA MALAT1 and HIF-1α in colon tissues.
CONCLUSIONS: The anti-UC effect of PRA by improving intestinal mucosal microcirculatory disorders was first reported in this study. PRA deactivated the lncRNA MALAT1/HIF-1α pathway, inhibited endothelial angiogenesis, restored intestinal mucosal microvascular homeostasis, improved microcirculatory disorders, and alleviated the symptoms of DSS-induced UC in rats.
PURPOSE: To examine how PRA affects UC induced by dextran sulfate sodium (DSS) and the mechanism of its effects.
METHODS: The primary active components of PRA were identified using high-performance liquid chromatography (HPLC), and network pharmacology techniques were used to predict the possible targets of action and signaling pathways in treatment for UC. A model of UC was established in vivo using rats, and a PRA intervention was performed. The amounts of cytokines in the colonic tissues and serum were measured using enzyme-linked immunosorbent assay (ELISA). The permeability of the intestinal mucosa was measured using a fluorescein isothiocyanate (FITC)-dextran assay and western blot. A PeriCam PSI system was used to view the microcirculation of the intestinal mucosa, and immunohistochemistry and immunofluorescence stains were used to detect angiogenesis. An electron microscope was used to observe the damage to the endothelium of the colon. Western blot and immunohistochemistry analyses were used to evaluate the protein expression of hypoxia-inducible factor-1 alpha (HIF-1α) in colon tissues, and qRT-PCR was used to assess the lncRNA expression of MALAT1.
RESULTS: HPLC identified 10 main active components of PRA, and the network pharmacology results showed that the treatment of UC with PRA was associated with the HIF-1 signaling pathway. The results of animal experiments revealed that PRA significantly improved the pathological damage to the colon and the microcirculatory issues in the intestinal mucosa. PRA also inhibited colonic endothelial cell damage and angiogenesis, which may be related to the inhibition of the increased expression of lncRNA MALAT1 and HIF-1α in colon tissues.
CONCLUSIONS: The anti-UC effect of PRA by improving intestinal mucosal microcirculatory disorders was first reported in this study. PRA deactivated the lncRNA MALAT1/HIF-1α pathway, inhibited endothelial angiogenesis, restored intestinal mucosal microvascular homeostasis, improved microcirculatory disorders, and alleviated the symptoms of DSS-induced UC in rats.