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??OBJECTIVE To investigate the protective effect and possible mechanism of Rhizoma Coptis(RC) on lipopolysaccharide(LPS)-induced inflammatory injury in rat hepatocytes(BRL). METHODS LPS-induced BRL cells injury model was established in vitro, then the damaged cells were given different interventions and treatment with 0.175, 0.1 mg?? mL^-1 RC aqueous extract as the test drug, and dexamethasone(Dex) as positive control drug. The optimal test doses of LPS and RC aqueous extract were selected and determined by cell counting kit-8(CCK-8), the cellular apoptosis rate was determined by flow cytometry, TLR4/NF-??B and TLR4/IRF3 signaling pathways and the mRNA level of related inflammatory mediators(TNF-??, IL-1??, IL-6) were detected by RT-PCR, the NF-??B p65 protein expression was analysed by Western blot and immunofluorescence techniques. RESULTS ??Compared with normal control group, 0.1 mg??mL^-1 LPS affected on BRL cells for 24 h, the cell survival rate was decreased significantly(P<0.01), the apoptotic rate increased significantly(P<0.01), the mRNA level of TLR4, NF-??B, IRF3, TNF-??, IL-1??, IL-6 were significantly increased(P<0.01), and the NF-??B p65 protein expression was increased. ??Compared with the model group, 0.1 and 0.175 mg??mL^-1 RC affected on LPS-induced BRL cells for 24 h, the survival rate of BRL cells was increased significantly(P<0.05), the apoptotic rate decreased significantly(P<0.01), the mRNA level of TLR4, NF-??B, IRF3, TNF-??, IL-1??, IL-6 and the NF-??B p65 protein expression were decreased significantly(P<0.01). CONCLUSION Rhizoma Coptis has obviously protective effect on LPS-induced inflammatory injury in rat hepatocytes(BRL), the mechanism of which may be related with inhibiting apoptosis, reducing the release of inflammatory factors such as TNF-????IL-1?? and IL-6, blocking NF-??B p65 protein nuclear translocation, interfering the R4/NF-??B and TLR4/IRF3 signaling pathway.     

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??OBJECTIVE To observe the effect of chlorogenic acid on the secretion of inflammatory cytokines and regulation mechanism of P38MAPK, NF-??B signaling pathway in human hepatic stellate cells induced by TGF-??1. METHODS Different concentrations of CGA worked in normal and activated hepatic stellate cells to make sure the appropriate drug concentration.The exponential growth phase cells were randomly divided into normal HSC group, normal HSC+CGA group, after cultured 48 h, the cells were cultured with 0??50??100 mg??L^-1 CGA for 24 h; HSC(TGF-??1) group?? HSC(TGF-??1 + CGA) group: after 24 h, the cells were induced by 10 ??g??L^-1 TGF-??1 for 24 h, and then cultured with 0, 50, 100 mg??L^-1 CGA for 24 h. The expression of ??-SMA protein was detected by immunocytochemistry, the expression of p-P38, P65 protein was detected by Western-blot, the expression of TNF-??, IL-6 mRNA was detected by real time quantitative PCR, and the content of TNF-??, IL-6 in the supernatant was detected by ELISA method. RESULTS The appropriate concentrations of CGA were 50 and 100 mg??L^-1, these concentration has no effect on normal HSC(P>0.05); after stimulation by TGF-??1, the expression of ??-SMA, p-P38, P65, TNF-??, IL-6 was increased(P<0.01), when activated HSC cells were treated with 50 and 100 mg??L^-1 CGA, the expression of ??-SMA, p-P38, P65, TNF-??, IL-6 was decreased(P<0.05, P<0.01). CONCLUSION CGA can inhibit the proliferation of activated HSC, regulate the secretion of inflammatory factors such as TNF-??, IL-6 by P38MAPK and NF-??B signaling pathway, inhibit the occurrence of liver fibrosis.     

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??OBJECTIVE To investigate the effect of ??-secretase inhibitor DAPT in inflammation-induced brain white matter injury in neonatal mice.METHODS Sixty C57BL/10J neonatal mice are randomly divided into control group, control+DAPT (10 mg??kg^-1) group, inflammation (LPS) group, LPS+DAPT group (inflammation exposure after 10 mg??kg^-1 DAPT treatment). All neonatal mice were killed and brain was removed to the following observation and detection:at P5, the mRNA expression variation of IL-1??, IL-8,TNF-??,Hes1 and NICD by Real-time PCR methods. Oligodendrocytes were identified by immunofluorescence staining. Myelin basic protein (MBP) protein expression was detected by Western blot assay.RESULTS LPS group showed brain injury characterized by inhibition of brain development. There were significant differences in mRNA expression of IL-1??, IL-8, TNF-??, Hes1 and NICD between LPS+DAPT group and LPS group (P<0.05), and the mRNA expression of IL-1??, IL-8,TNF-??,Hes1 and NICD in inflammation-treated were significantly increased than control group (P<0.05). The results showed more expression of MBP in LPS+DAPT group compared with LPS group (P<0.05). Compared with the blank control group, which was obviously decreased after 48 h of inflammation (P<0.05).CONCLUSION Inflammation leads to abnormal of notch signal expression in neonatal mice, and which is shows inflammation involved in brain damage.Its mechanism is probably associated with the maturation of oligodendrocytes.     

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??OBJECTIVE To study the effect of kangfuxin on damp-heat syndrome combined with TNBS-induced ulcerative colitis in rats and to explore its mechanism. METHODS Rat model of damp-heat was established by high-fat and high-sugar diet, and then combined with TNBS to establish rat model of damp-heat, respectively, to give sulfasalazine, rehabilitation, high, medium and low dose enema, by measuring disease activity index(DAI), colonic mucosal injury index(CMDI) and histopathological score(HS). The levels of IL-8, IL-17 and IL-2, MPO, EGF and TNF-?? in serum were measured by enzyme-linked immunosorbent assay(ELISA). RESULTS Compared with the model control group, the high dose group can significantly reduce the DAI, HS and CMDI scores of the damp-heat type UC rats(P<0.01, P<0.05). Each group type can reduce the heat UC rat serum IL-8, IL-17 and expression of MPO,TNF-?? in colon tissue, increases, the expression of rat IL-2 EGF(P<0.01). CONCLUSION Kangfuxin has a certain therapeutic effect on damp-heat type UC rats, and its mechanism may be related to down-regulating the expression of IL-8, IL-17,MPO and TNF-??, up-regulating the expression of IL-2 and EGF.     

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??OBJECTIVE To study the immunoregulatory effect of Dendrobium officinale polysaccharide (DOP) obtained by step ethanol precipitation on macrophages and explore its action mechanisms. METHODS Step ethanol precipitation method was used to get DOPs of different molecular weights, MTT method was used to detect the protective effect of DOP on macrophages induced by LPS, neutral red method was used to detect the phagocytosis activity of macrophages, ELISA method was used to detect the contents of TNF-??, IL-6, and TGF-??1, and Griess method was used to detect the NO release quantity. RESULTS The yield of DOP was the largest when the ethanol concentration was 75%. DOP could promote the proliferation and phagocytosis activity of RAW264.7 cells, reduce the release of TNF-??, IL-6 and NO, and promote the secretion of TGF-??1 and the proportion of M2 significantly (P<0.01). CONCLUSION Dendrobium officinale polysaccharide has immune regulation effect on RAW264.7 cells, and the mechanism may be related to the promotion of cell phagocytosis activity, inhibition of inflammatory factor release, promotion of TGF-??1 secretion, and increase of the proportion of M2.     

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??OBJECTIVE To observe the influence of safflower yellow(SY) on inflammatory injury in cortex of APP/PS1 double Alzheimer??s disease(AD) transgenic mice.METHODS Six-month-old APP/PS1 transgenic male mice were used in the study.The mice were randomly divided into five groupsmodel group, galanthamine group,high,middle and low dose groups of Safflower Yellow,and wild-type mice with same age were selected into normal control group. Each group mice were performed Morris water maze test after given different drugs by gavage for three months. The level of IL-1??, IL-4, IL-10, IFN-?? and iNOS in cortex were detected by ELISA. RESULTS Compared with wild-type controls, the ability of learning and memory were decreased in the model group. The level of IL-1??, IFN-?? and iNOS increased as well as the expression of IL-4, IL-10 decreased(P<0.01). After SY treatment, the learning and memory abilities of middle dose group were elevated (P<0.01); it could obviously down-regulate the expression of IL-1??, IFN-??, iNOS and up-regulate the expression of IL-4 and IL-10 (P<0.01). High and low dose groups could obviously down-regulate the expression of IFN-??, iNOS and up-regulate the expression of IL-10 (P<0.01). High dose group does had obvious effect of up-regulating the expression of IL-4 (P<0.01), Both of High and low dose groups didn??t have statistical significance on the expression of IL-1??.CONCLUSION Safflower Yellow could improve the ability of learning and memory and exert protective effects on inflammation damage in the cortex of APP/PS1 transgenic mice.     

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??OBJECTIVE To clarify the effect of total glucosides from paeony(PTG) on irritable bowel syndrome (IBS), and to explore the molecular mechanism of PTG on alleviating diarrhea symptoms and abdominal pain.METHODS The diarrhea model was conducted by exposing rat to restraint stress stimulation and bellyache model was conducted by subcutaneous injection of neostigmine to mice. Based on these two models, the curative effect of PTG on IBS was investigated. To investigate the regulative effects of PTG on Caco-2 cells, the Caco-2 monolayer cell model with barrier dysfunction was established by trypsin stimulation, and the inflammatory Caco-2 cell model was established by interleukin-1?? (IL-1??) stimulation.RESULTS PTG could significantly reduce the frequency of defecation in diarrhea rat model (P<0.05) and relieve abnormal bowel movements in bellyache mice model (P<0.05). After PTG treatment, the TEER value of Caco-2 monolayer was significantly increased (P<0.01), the transmittance of fluorescence yellow was significantly decreased (P<0.001) and the expression of tight junction (ZO-1)protein was notably up-regulated (P<0.001). In addition, the gene and protein expression of nuclear factor profilin kappa B(I??B??)in inflammatory Caco-2 cell model was significantly improved (P<0.001) after PTG treatment.CONCLUSION PTG significantly ameliorates IBS symptoms by protecting the barrier function of Caco-2 cell monolayer and relieving inflammation of Caco-2 cells.