Exploring the role and mechanism of armillariella tabescens polysaccharides interference in 5-FU-induced intestinal mucosal injury based on ARRB1 / 安徽医科大学学报
Acta Universitatis Medicinalis Anhui
; (6): 1743-1749, 2023.
Article
in Zh
| WPRIM
| ID: wpr-1038361
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ABSTRACT
Objective @#To investigate the effect and mechanism of ARRB1 on Armillariella tabescens polysaccharides reversal of 5-fluorouracil ( 5-FU ) -induced chemotherapeutic intestinal mucosal injury.@*Methods @# Twelve ARRB1 knockout ( ARRB1 -/ - ) and wild-type ( WT) C57BL /6 mice were randomly divided into Control,Model and ATPS groups (200 mg / kg) ,respectively.5-FU (50 mg / kg) was injected intraperitoneally for 7 days to establish a model of chemotherapeutic intestinal mucosal injury.The histopathological damage of jejunum was evaluated by HE staining ; the activity of serum superoxide dismutase (SOD) and diamine oxidase (DAO) was measured by kits ; the expression of tight junction protein (TJ) markers ZO-1,Occludin,Claudin-1 and proliferation-associated protein Ki-67 was detected by immunohistochemistry.Crypt isolation and organoid culture were used to detect the growth status of small intestinal organoids. @*Results @#5-FU chemotherapy reduced body weight,aggravated histopathological damage in small intestine,decreased SOD level,TJ protein and Ki-67 protein expression,increased serum DAO level,decreased spherical structure formation rate and organoid formation rate ; compared with the model group,after ATPS treatment,WT mice recovered body weight,decreased pathological damage,increased serum SOD level,TJ protein and Ki-67 protein expression,DAO levels decreased,and the rates of spherical structure for- mation and organoid formation were significantly higher.However,ARRB1 -/ - mice failed to reverse the effect of 5- FU after ATPS treatment.@*Conclusion @#ATPS reverses 5-FU-induced intestinal mucositis through the protective effects of ARRB1 on intestinal barrier and organoid growth.
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Index:
WPRIM
Language:
Zh
Journal:
Acta Universitatis Medicinalis Anhui
Year:
2023
Type:
Article