Mechanistic Study of Qingchang Huashi Recipe Regulating the Nrf2/ARE Pathway to Alleviate Ulcerative Colitis
Ulcerative colitis(UC)is a type of idiopathic chronic inflammatory bowel disease that tending to recur and significantly affecting the health and quality of life of patients.This study utilized a mouse model of UC,focusing on the oxidative stress pathway,to investigate the mechanisms through which Qingchang Huashi Recipe(QHR)alleviates UC.The primary methods involved inducing UC in mice using Dextran Sodium Sulfate(DSS).Daily measurements of mouse body weight,observation and recording of fecal characteristics and bleeding were conducted.After the treatment,the mouse colon length was measured,and colon tissue was collected.Various parameters were evaluated at the genetic,protein,and pathological levels.A portion of the collected colon tissue was subjected to qRT-PCR to assess the expression of HO-1,NQO-1,Keap1,and Nrf2 in colon tissue.Another portion was subjected to nuclear magnetic resonance metabolomics analysis to examine changes in colon metabolites among different groups and perform multivariate statistical analysis.A third portion was used to prepare colon pathological sections for hematoxylin and eosin(HE)staining and immunohistochemistry.HE staining was used to assess the pathological inflammation in colon tissue,and immunohistochemistry was employed to determine the expression of Keap1 and Nrf2 in colon tissue.The results demonstrated that QHR could increase the survival rate of mice with UC.Compared to the normal control group(Ctrl),mice in the DSS model group exhibited decreased body weight,shorter colon length(P<0.05),higher colon tissue pathological inflammation scores(P<0.05),and decreased expression of antioxidant response elements,all of which were statistically significant(P<0.05).After QHR administration,mice showed increased body weight,longer colon length(P<0.05),lower colon tissue pathological inflammation scores(P<0.05),and higher expression of HO-1,NHO-1,Nrf2,with a decrease in Keap1 expression,all of which were statistically significant(P<0.05)compared to the DSS group.This study found that QHR alleviated mucosal damage in the intestine caused by excessive oxidation by increasing Nrf2 expression and subsequently upregulating ARE-related molecules.