ABSTRACT
OBJECTIVE:To study the preventive effect and mechanism of Wei medicine Kunlun snow chrysanthemum polysac-charides(KSCP)on carbon tetrachloride(CCl4)-induced acute liver injury in mice. METHODS:96 mice were randomly divided in-to normal group(normal saline),model group(normal saline),Biphenyl diester dropping pill(positive control,1.5 mg/10 g)and KSCP low-dose,medium-dose,high-dose groups (0.3,0.6,1.2 mg/10 g),16 in each group,with intragastric administration, once a day,for 10 d. Except for normal group,mice in other groups were intraperitoneally injected 1%CCl4 rapeseed oil solution to induce liver injury. After 24 h of modeling,the levels of alanine aminotransferase (ALT),aspartate aminotransferase (AST),tu-mor necrosis factor α(TNF-α),interleukin 1(IL-1)in serum,levels of malondialdehyde(MDA),superoxide dismutase(SOD) in liver tissue were detected;the liver,spleen indexes were calculated. Pathological changes of liver tissue were observed,patho-logical scoring was conducted. The protein expressions of apoptosis-related genes Caspase-3,Bcl-2,Bax in liver tissue were detect-ed. RESULTS:Compared with normal group,levels of ALT,AST,TNF-α,IL-1 in serum,MDA level in liver tissue and liver, spleen indexes in model group were obviously increased(P<0.01);SOD level in liver tissue was decreased(P<0.01);pathologi-cal changes in hepatocellular necrosis,degeneration and inflammatory cell infiltration,and pathological score in model group was obviously increased(P<0.01);caspase-3 protein expression and Bcl-2/Bax ratio in liver tissue in model group were obviously de-creased (P<0.01). Compared with model group,above-mentioned indexes in each administration group were obviously improved (P<0.05 or P<0.01). CONCLUSIONS:KSCP has certain preventive effect on CCl4-induced acute liver injury in mice,and its mechanism may be associated with anti-oxidation,anti-inflammation and regulation of apoptosis-related protein expressions.
ABSTRACT
Objective To investigate the immunoregulatory effect of Fasudil-modified macrophages on cell transferred experimental autoimmune encephalomyelitis ( EAE) in a mouse model.Methods Fe-male C57BL/6 mice were immunized with MOG35-55 to establish the model of EAE.The encephalomyelitic mononuclear cells ( MNCs) were isolated from spleen of mice with EAE on day 9 after immunization and treated with or without Fasudil for 72 h in vitro.Several assays including the flow cytometry analysis, Griess reaction and ELISA were performed to analyze the M1 and M2 phenotypes of macrophages, the production of NO and the levels of cytokines, respectively.The cultured MNCs (5×107 cells) were resuspended in 500μl of PBS and transferred into na?ve C57BL/6 recipients via intraperitoneal injection.Two groups including the PBS-MNCs group and the Fasudil-MNCs group were set up.The body weights and clinical scores of the mice in each group were recorded in every other days after the induction of EAE in the recipients.Results The Fasudil treated MNCs affected the induction of EAE in adoptive cell transferred mice.The expression of CD16/32, iNOS and IL-12 on F4/80-macrophages were decreased, while the expression of CD206, CD23 and IL-10 on F4/80-macrophages were increased upon the treatment of Fasudil, indicating that Fasudil im-proved the differentiation of macrophages from M1 to M2 phenotypes.Moreover, Fasudil inhibited the pro-duction of NO and enhanced the expression of Arginase-1.Conclusion Fasudil ameliorated the clinical se-verity of EAE in mice by promoting the transformation of macrophages from M1 to M2 phenotype.
ABSTRACT
Objective To investigate the anti -allergic effects of Xitare tablets combined with external use of Xitare Oint-3Gussinye Mment.MethodsSynlogousratmodelsofdermalsensitivity,mousemodelsofDNCB-induceddelayedhypersensitivity,ratmodelsofmastocyticdegranulationandguineapigmodelsofhistamine-phosphate-induceditchingreactionwereap-plied.ResultsXitaretablets(1.75,3.5,7.0g/kgbodyweight,bid,ig)combinedwithexternaluseofXitareOint-ment(0.7,1.4,2.1g/pertime,qd)obviouslycounteractedtheallergicreactioninratswithdermalsensitivity(P