| Objective: To investigate the effect and mechanism of Ginsenoside Rg1againstinterleukin-1beta (IL-1β)–induced apoptosis in rat articular chondrocytes.Method: Firstly, we determined the optimal concentration of Rg1to protectchondrocytes apoptosis. Experimental groups were set as follows. Group1:chondrocytes were exposed to10ng/ml IL-β for h to create apoptosis model.Group2-5: chondrocytes were exposed to different concentrations Rg1(0.1，1，10and100μg/ml) for2h then10ng/ml IL-β was added Group6: chondrocytes were leftuntreated. The p-Akt level induced by Rg1was detected by Western blot.Secondly, the effect of Rg1against chondrocyte apoptosis was assessed byterminal dexynucleotidyl transferase mediated dUTP nick end labeling (TUNEL)staining. Experimental groups were set as follows. Group1: chondrocytes wereexposed to10ng/ml IL-β for4h to create apoptosis model. Group2: chondrocyteswere exposed to10μg/ml Rg1for2h then10ng/ml IL-β was added Group:chondrocytes were left untreated.Thirdly, Western blot was employed to determine the influence of Rg1onPI3K/Akt/mitochondria signaling of chondrocyte. Experimental groups were set asfollows. Group1: chondrocytes were exposed to10ng/ml IL-β for h to createapoptosis model. Group2: chondrocytes were exposed to10μg/ml Rg1for2h then 10ng/ml IL-β was added Group: chondrocytes were exposed to10μg/ml Rg1for24h. Group4: chondrocytes were co-cultured with25μmol/ml LY294002and10μg/ml for2h and IL-β was added for another24h. Group5: chondrocytes were leftuntreated.Results: The first step showed Rg1at concentrations of1-100μg/ml canincrease the level of p-Akt in chondrocytes (P <0.05). No significant difference ofp-Akt expression was found between10and100μg/m Rg1(P>0.05).The second step showed Rg1can protect chondrocyte apoptosis induced byIL-β The TUNEL positive cell rate in group of the model group was higher than thecontrol, and The TUNEL positive cell rate in the experimental group was lower thanthe model group (P <0.05).The third step showed Rg1can influence on PI3K/Akt/mitochondria signaling ofchondrocyte. Compared with the control, expressions of p-Akt, Bcl-2andmitochondrial cytochrome C were inhibited while expressions of Bax, cytoplasmiccytochrome C and cleaved caspase-3were increased in the model group (P <0.05).Compared with the model group, expressions of p-Akt, Bcl-2and mitochondrialcytochrome C were recovered while expressions of Bax, cytoplasmic cytochrome Cand cleaved caspase-3were reduced in the experimental group (P <0.05). Theprotective effect of Rg1can be inhibited by the LY294002.Conclusion: Rg1can protect rat articular chondrocyte from apoptosis inducedby IL-1β via PI3K/Akt signaling pathway. Objective：To determine the efficacies of different preparations of glucosaminefor the treatment of osteoarthritis (OA).Methods：Systematic searches of the bibliographic databases Medline, Embase,the Cochrane Central Register of Controlled Trials, and the Cochrane Database ofSystematic Reviews for randomized, double-blind, placebo-controlled trials (RCTs)concerning glucosamine treatment of hip or knee OA. All included trials wereevaluated by a quality assessment instrument developed by Jadad. Effect size (ES)was estimated using Cohen’s standardized mean difference Consistency wasevaluated via the I2index. The outcome measures was pain reduction and physicalfunction improvement with glucosamine compared to placebo. Outcomes wereextracted in terms of efficacy including pain assessed by the visual analog scale (VASpain), the Western Ontario McMaster University Osteoarthritis Index (WOMAC pain),and the Lequesne Index (LI). Analyses were performed by stratifying the availabledata according to joint affected, allocation concealment, ITT analysis, and trialduration. publication bias was investigated using both the Egger test and a funnelplot.Results：A total of19articles (3159subjects) were therefore selected forinclusion in the meta-analysis. Fifteen trials used GS, and four used GH. Seventeenstudies contributed to the meta-analysis of pain-reduction outcomes, with notreatment ES favoring glucosamine compared to placebo (-0.16,95%CI-0.34,0.01)and I2of78.3%. Thirteen GS studies showed no treatment effects (ES-0.22,95%CI -0.48,0.04) and I2was82.3%. A combined ES of-0.03,(95%CI-0.14,0.08) in fourGH studies showed no significant effect versus placebo, with a heterogeneity of zero.Subgroup analysis demonstrated estimates of ESs varied to some degree dependingon trial design. ES of trials lasting less than24weeks was-0.38(95%CI-0.99,0.23)and the I2was88.5%. No significant treatment ES (-0.09(95%CI-0.21,0.03)) wasfound in trials lasting longer than24weeks compared to placebo, with aheterogeneity of zero. GS showed no significant benefit versus placebo in terms of LIreduction when administered for less than24weeks (ES-0.55(95%CI-1.22,0.11)),and the degree of heterogeneity was92.9%. Pooling data for the two studies withdurations of more than24weeks produced a moderate ES of-0.36(95%CI-0.56,-0.17), with no heterogeneity.Conclusion：The results of this study support the fact that GS treatment for morethan6months improves joint function, but not joint pain, in patients with knee OA.Further trials of GS for the treatment of knee or hip OA are needed to confirm thisapparent lack of benefit of GS. GH is ineffective for relieving pain in OA patients. |
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