Objective To evaluate the effects of magnesium sulphate on the analgestic efficacy of nerve block analgesia with ropivacaine. Methods Sixty cases who used femoral nerve block analgesia after unilateral total knee arthroplasty under the general anesthesia were selected,and according to digital table they were randomly divided into two groups( n=30 each):magnesium sulfate plus ropivacaine( group M) and ropivacaine( group C) . The solution (20mL) of 0. 2% ropivacaine and 0. 15% magnesium sulphate were administered to group M,and 20mL solution of 0.2% ropivacaine was given to the group C. The pain score was measured by visual analogue scale(VAS). The supplementary usage and cumulative dosage of morphine were recorded and the analgesia relevant complications were observed. Results The results of this study indicated that 4h,8h,12h and 24h after the operation,the VAS scores had no statistically significant difference ( all P > 0. 05 ) at rest, which in group M was significantly decreased compared with group C at 12h(t=2. 800,P=0. 009) and 24h(t=2. 934,P=0. 012) after treated with continuous passive motion ( CPM) postoperatively. The cumulative dosages of morphine when patients undergo CPM of knee joint in group M were (2.78 ±0.32)mg,(2.05 ±0.16)mg,respectively,which were significantly lower than those in the groupC[(4.10±0.85)mg,(2.44±0.25)mg](t=7.960,2.632,all P<0.05).No obvious analgesia relevant complications occurred in both two groups. Conclusion Magnesium sulphate can enhance the efficacy of postopera-tive femoral nerve block analgesia with ropivacaine, reduce the usage of morphine without increasing the analgesia relevant complications.

The high- and the low-molecular weight hyaluronic acids (HMW-HA and LMW-HA, respectively) showed different biological activities in inflammation. However, the role of LMW-HA in inflammatory response is controversial. In this study, we aimed to investigate the effect of bioactive hyaluronan (B-HA) on lipopolysaccharide (LPS)-induced inflammatory responses in human macrophages and mice. B-HA was produced from HA treated with glycosylated recombinant human hyaluronidase PH20. Human THP-1 cells were induced to differentiate into macrophages. THP-1-derived macrophages were treated with B-HA, LPS, or B-HA + LPS. The mRNA expression and the production of inflammatory cytokines were determined using quantitative real-time PCR and enzyme-linked immunosorbent assay. The phosphorylation levels of proteins in the nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and IRF-3 signaling pathways were measured using Western blot. The in vivo efficacy of B-HA was assessed in a mouse model of LPS-induced inflammation. Results showed that B-HA inhibited the expression of TNF-α, IL-6, IL-1, and IFN-β, and enhanced the expression of the antiinflammatory cytokine IL-10 in LPS-induced inflammatory responses in THP-1-derived macrophages and in vivo. B-HA significantly suppressed the phosphorylation of the TLR4 signaling pathway proteins p65, IKKα/β, IκBα, JNK1/2, ERK1/2, p38, and IRF-3. In conclusion, our results demonstrated that the B-HA attenuated the LPS-stimulated inflammatory response by inhibiting the activation of the TLR4 signaling pathway. B-HA could be a potential anti-inflammatory drug in the treatment of inflammatory disease.
Animals ; Cytokines ; Hyaluronic Acid ; Lipopolysaccharides ; Mice ; NF-kappa B/metabolism* ; Signal Transduction ; Toll-Like Receptor 4