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BACKGROUND: In recent years, extensive studies on the pain management after total knee arthroplasty (TKA) have identified different ways of analgesia. Among which, femoral nerve block (FNB) is the standard antalgic method post-TKA for its effective analgesia, but it may reduce the muscle strength of the quadriceps after TKA and cause serious consequences. Adductor canal block (ACB) is a novel antalgic method that provides fast functional recovery and good ability of pain control after TKA. OBJECTIVE: To compare the functional recovery and ability of pain control of ACB and FNB after TKA through a meta-analysis. METHODS: Databases of WanFang, CNKI, PubMed, Web of Science, and Embase were searched for the literature concerning the analgesia and functional recovery after TKA published before March 2017. The articles were evaluated according to the Cochrane system and a meta-analysis was conducted on Revman 5.1. RESULTS AND CONCLUSION: (1) Twelve articles were included involving 802 patients with 872 knees. (2) Meta-analysis results showed that compared with FNB, ACB significantly reduced the Visual Analogue Scale scores at rest at 8 hours postoperatively (P < 0.001) and significantly improved the muscle strength of quadriceps femoris (P < 0.001) and motor capacity (Timed Up and Go test) (P < 0.05); but the scores at rest at 24 and 48 hours postoperatively, and the scores in activity at postoperative different time points, usage of opioids, and hospitalization time did not differ significantly between two groups. (3) ACB can achieve better analgesia at the early period (8 hours) after TKA, better motor capacity and stronger muscle strength of the quadriceps femoris; thereafter, it is a substitute for FNB after TKA.
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Aim To explore the mechanism of the protective effect of curcumin on advanced glycation end products (AGEs)-induced chondrocyte apoptosis and mitochondrial dysfunction whether by elevating peroxisome proliferators-activated receptor-γ (PPARγ) or not.Methods The ratio of apoptotic cells was assayed by TUNEL;the mitochondrial membrane potential(△Ψm) was evaluated by Rhodamine-123 fluorescence.The ATP content was assayed by related kits.The activity of caspase-3 was detected by spectrophotometry.The expression of cytochrome C,Bax,and Bcl-2 was detected by Western blot.The PPARγ expression was determined by Western blot and real-time PCR;in addition,its activity was assayed by DNA-binding method.Results AGEs could induce chondrocyte apoptosis and up-regulate the levels of cytochrome C and caspase-3.Simultaneously,AGEs decreased the levels of △ Ψm and ATP production.Mitochondrial permeability conversion pore inhibitor cyclosporine A could significantly protect the cells from apoptosis.In addition,both PPARγ specific agonist pioglitazone and curcumin significantly inhibited AGEs-induced chondrocytes apoptosis and mitochondrial dysfunction.However,pretreatment with PPARγ specific inhibitor GW9662 (10 μ mol · L-1) could significantly antagonize the protective effect of curcumin on mitochondrial damage induced by AGEs.Curcumin could also significantly increase PPARγtranscriptional activity induced by AGEs,together with a significant induction of PPARγprotein and mRNA expression.Conclusion Curcumin could effectively protect AGEs-induced chondrocyte mitochondrial dysfunction by upregulating PPARγ,thus protecting chondrocytes from apoptosis.