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??OBJECTIVE To investigate the anti-inflammatory effects of extract of Scutellaria baicalensis Georgi (SGE) and underlying mechanism by using LPS-induced microglial BV2 cells. METHODS MTT assay was used to observe the cell viability. The content of NO in cell supernatant was measured by Griess reagent. The levels of IL-1??, IL-6 and TNF-?? were detected by ELISA kits. The intracellular TLR4 expression was assayed by Western blotting. RESULTS The levels of NO, IL-1??, IL-6 and TNF-?? were significantly increased induced by LPS in the supernatant of BV2 cells (all P<0.01). However, co-treatment with SGE 100 ??g??mL^-1 significantly decreased the production of related inflammatory factors including NO (P<0.01), IL-1??(P<0.01), IL-6 (P<0.01) and TNF-?? (P<0.05). Furthermore, SGE significantly inhibited the TLR4 expression induced by LPS in BV2 cells. CONCLUSION SGE is able to alleviate LPS-induced inflammatory responses in BV2 cells through down-regulation of TLR4 protein expression suggesting that SGE has therapeutic potential for the treatment of neuroinflammatory diseases.     

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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 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 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 compare the chemical composition and therapeutic effect between Prunella vulgaris L stem leaf and ear, thus to provide evidence for judging whether the stem leaf of Prunella vulgaris L can substitute the ear as an herbal medicine. METHODS Aqueous extracts of the stem leaf and ear of Prunella vulgaris L from different producing areas were analyzed with HPLC-ESI-MSⁿ. The anti-inflammatory effects were observed by inflammatory models of ear edema induced by dimethylbenzene in mice and hind paw edema induced by carrageenan in rats.Enzyme-linked immunosorbent assay (ELISA) was used to detect the plasma level of TNF-?? and antioxidant activities were detected by ABTS method. RESULTS Prunella vulgaris L stem leaf and ear were not significantly different in chemical composition, both of which contained mainly triterpenoids, flavonoids, phenolic acids and other substances. Compared with the model group, Prunella vulgaris L ear significantly reduced the hind paw edema in rats induced by carrageenan from 1 h after oral administration (P<0.05), while the onset time of stem leaf was later than 1 h.Both groups could significantly reduce the ear edema in mice induced by dimethylbenzene(P<0.01). The TNF-?? levels in the Prunella vulgaris L stem leaf and ear groups [(24.16??1.24) and (24.33??2.36 )ng??mL^-1] were lower than that in the model group [(31.34??1.94) ng??mL^-1] (P<0.01).Prunella vulgaris L stem leaf and ear groups showed strong antioxidant activities in the ABTS^??+ scavenging test. CONCLUSION The contents of the main constituents in Prunella vulgaris L stem leaf and ear have significance differences.The RESULTS of animal tests indicate that the aqueous extracts of Prunella vulgaris L stem leaf and ear have significant anti-inflammatory and antioxidant effects.     

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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 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.     

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??OBJECTIVE To study the effects and mechanisms of apple polysaccharides(AP) on tumorigenesis in a mouse model of colitis-associated colon cancer. METHODS AP was obtained from apple pomace and its protective efficacy was evaluated on carcinogenesis in a mouse model of colitis-associated colon cancer induced by azoxymethane (AOM) and dextran sodium sulfate (DSS). The effects of AP on TLR4/MyD88/NF-??B pathway were measured using immunohistochemistry , ELISA and Western blot.The serum were collected and TNF-?? was measured by ELISA kits. RESULTS After 20 weeks of continuous treatment, the incidence of colon cancer formation was 95% in the mice treated with AOM/DSS (model group), and these reduced to 26%, 10% and 5% in AP (1.25%, 2.5% and 5%) treatment group respectively. Western blot analysis demonstrated that TLR4 (membrane protein), MyD88, NF-??B p65 (nuclear protein) expression decreased significantly at protein level; and the secretion of TNF-?? decreased in control group(P<0.05). CONCLUSION AP could protect ICR mice from CACC effectively and the possible mechanism may be related to the inhibition of TLR4/MyD88/ NF-??B pathways.     

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??OBJECTIVE To study the effects of fibroblast growth factor-21(FGF-21) on acute inflammation induced by lipopolysaccharide (LPS)and its mechanism. METHODS Mouse model of acute inflammation was established by injection of LPS and treated with FGF-21 at high, medium and low doses, the pathological changes were detected with HE staining, the expression level of TNF-??, IL-1??, IL-6 and IL-17 in serum and peritoneal macrophage were determined by ELISA and Real-time PCR. NF-??B p65 in macrophage cells was analyzed by confocal laser scanning microscope and Western-blotting. RESULTS FGF-21 treatment reduced lung damage and inflammatory cell infiltration and decreased the expression level of TNF-??, IL-1??, IL-6 and IL-17 in both serum and peritoneal macrophage. The results of confocal laser scanning microscope and Western-blotting both showed that FGF-21 could inhibit NF-??B transferring to the nucleus. CONCLUSION FGF-21 could regulate the immune system by acting on macrophage. Relieving the inflammatory response in mice through NF-??B signal pathway may be one of the mechanisms FGF-21 regulating immune system.