| Purpose:Part one To discuss the theoretical basis of KJAKD in the treatment of ulcerative colitis(UC).Part two To reveal the repair mechanism of KJAKD in the treatment of intestinal damaged mucosa of UC rats.Method:This study is divided into theoretical and experimental research.Part one Theoretical study Professor Liu Yuedong's understanding of etiology and pathogenesis of UC is elaborated in detail.Based on this,the basic principles of UC treatment are put forward,and the summary and modern pharmacological research of KJAKD are summarized.Part two Experimental study This study used three trinitrobenzene sulfonic acid(TNBS)/ ethanol twice phlogogenic method to establish the rat model of UC,to observe the effect of KJAKD in general health and morphology of colonic tissue of UC rats,and to use ELISA,RT-PCR,Western blot detection technology to analyze effects of KJAKD on TGF beta 1,b FGF,EGF,P-MEK,P-ERK of rats with UC.Results:Part one Theoretical study Professor Liu Yuedong believes that UC is the virtual reality syndrome.Spleen deficiency is the basis of its incidence.Toxic heat is intrinsic conditions of its incidence.Blood stasis is the pathological product of this disease.These are in accordance with the understanding of the etiology and pathogenesis of the medical practitioners in China.She advocates the treatment of invigorating spleen and nourishing qi,clearing heat and detoxifying,removing blood stasis and dredging collaterals.The modern pharmacological studies and previous experimental studies have shown that KJAKD has the effect of inhibitinginflammation and repairing intestinal mucosa damage.Part two Experimental study1.General situation Normal diet,normal stool,soft hair and luster,normal mental activity and a gradual increase in weight in the normal group.After two times of inflammation,the model rats were depressed,dark hair,watery,bright red blood in the stool,loss of appetite and weight loss and other symptoms.Give KJAKD,SASP and BPYCP after treatment,the symptoms of the three groups of rats improved gradually,and were better than the model group's.2.DAI score Compared with the normal group,the DAI score of the model group was significantly higher,and the difference was significant(P < 0.01).Compared with the model group,the DAI score of the KJAKD group,the SASP group all days and the BPYCP group given medicine 14 d and 21 d were decreased,the difference was statistically significant(P < 0.01).The DAI scores of the KJAKD group given medicine 1d,7d and 21 d were not significantly different from those in SASP group(P > 0.05),which were significantly lower than those in BPYCP group(P < 0.01 or P < 0.05).3.CMDI score Compared with the normal group,the CMDI score of the model group was significantly higher,and the difference was significant(P < 0.01).Compared with the model group,the CMDI scores of all the treatment groups were reduced,and the difference was statistically significant(P < 0.01).There was no significant difference in CMDI score between KJAKD group and SASP group(P > 0.05),which was significantly lower than that of BPYCP group(P < 0.05).4.Histopathological score Compared with the normal group,the histopathological score of the model group was significantly higher,and the difference was statistically significant(P < 0.01).Compared with the model group,the histopathological score of each treatment group was significantly lower,and the difference was statistically significant(P < 0.01).There was no significant difference in histopathologic score between KJAKD group and SASP group(P > 0.05),which was significantly lower than that in the group of BPYCP(P < 0.01).5.The content of TGF-beta 1 in serum and colon tissue Compared with the normal group,the content of TGF-beta 1 in the serum and colon tissues of the model group was significantly lower,and the difference was statistically significant(P < 0.01).The content of TGF-beta 1 in the serum and colon tissues of the rats in each treatment group was higher than that in the model group,and the difference was statistically significant(P < 0.01).The content of TGF-beta 1 in serum and colon tissue of KJAKD group was not significantly different from that of SASP group(P > 0.05),which was significantly higher than those in the BPYCP group,and the difference was statistically significant(P < 0.01).6.The expression of b FGF m RNA in colon tissue Compared with the normal group,the relative expression of b FGF m RNA in the colon tissue of the model group was significantly higher,and the difference was significant(P <0.01).Compared with the model group,the relative expression of b FGF m RNA in the colon tissue of the rats of each treatment group was significantly higher,and the difference was statistically significant(P < 0.01).The relative expression of b FGF m RNA in colonic tissue of KJAKD group was significantly higher than that of SASP group and BPYCP group(P <0.01).7.The expression of EGF m RNA in colon tissue Compared with the normal group,the relative expression of EGF m RNA in the colon tissue of the model group was significantly lower,and the difference was significant(P <0.01).Compared with the model group,the relative expression of EGF m RNA in the colon tissue of the rats of each treatment group increased significantly,and the difference was statistically significant(P < 0.01).The relative expression of EGF m RNA in colon tissue of KJAKD group was not significantly different from that of SASP group(P > 0.05),which was higher than that of BPYCP group(P < 0.05).8.The expression of p-MEK and p-ERK protein in colon tissue Compared with the normal group,the expression of p-MEK and p-ERK protein in the colon tissue of the model group was significantly higher,and the difference was statistically significant(P < 0.01).Compared with the model group,the expression of p-MEK and p-ERK protein in the colon tissue of the rats of each treatment group increased significantly,and the difference was statistically significant(P < 0.01).The expression of p-MEK and p-ERK protein in colonic tissue of KJAKD group was not significantly different from those in SASP group(P > 0.05),which were significantly higher than those in the BPYCP group(P <0.01 or P < 0.05).Conclusion:Part one Theoretical study Spleen deficiency is the basis of its incidence.Toxic heat is intrinsic conditions of its incidence.Blood stasis is the pathological product of this disease.Strengthening spleen and Invigorating Qi,clearing heat and detoxifying and removing blood stasis and dredging collaterals are its basic rules,which are the theoretical basis of KJAKD in the treatment of UC.Part two Experimental study1.KJAKD can relieve the intestinal inflammation in UC rats KJAKD can effectively improve the general condition,colonic morphology and pathological changes of colonic mucosa under light microscope of UC rats induced twice by TNBS/ ethanol,reduce the inflammatory response of the intestinal tract and promote the repair of damaged colon mucosa,so as to achieve the purpose of treatment.2.KJAKD can improve the content of TGF-beta 1 in the serum and colonic tissues of UC rats KJAKD can inhibit the inflammatory reaction by increasing the content of TGF-beta1 in the serum and colon tissue of UC rats,so as to maintain the balance of intestinal mucosal immune system,and promote ulcer healing.3.KJAKD can improve the expression of b FGF and EGF m RNA in the colon tissue of UC rats Through upregulation of b FGF and EGE m RNA expression in colon tissue,KJAKD can play a regulatory role of b FGF and EGF two kinds of growth factors,stimulate epithelial cell proliferation and angiogenesis,protect the intestinal mucosal barrier,and then promote the impaired mucosal repair,and ultimately achieve the purpose of treatment.4.KJAKD can improve the expression of p-MEK and p-ERK protein in the colon tissue of UC rats KJAKD can increase the expression of p-MEK and p-ERK protein in colon tissue of UC rats,activate the MEK/ERK signal transduction pathway,and then lead to the repair of intestinal damaged mucosa.In summary,the mechanism of KJAKD in the treatment of UC may be raising the content of TGF-beta 1 level,increasing the expression of b FGF and EGF genes,and activating of the MEK/ERK signaling pathway,thereby inhibiting the intestinal inflammation,protecting the intestinal mucosal barrier,promoting the intestinal mucosal repair,leading to the ulcer healing of UC. |
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