Objective To assess the clinical application of lysophosphatidic acid (LPA) as the early warning index for cerebral ischemic stroke (CIS). Methods Trials were collected through electronic searches of PubMed, The Cochrane Library, CBM, CNKI, Wanfang, and VIP (from the date of database establishment to June 2009). We screened the retrieved studies according to the predefined inclusion and exclusion criteria, evaluated the quality of the included studies, performed descriptive analysis and meta-analysis with The Cochrane Collaboration’s RevMan 4.2 software. Results A total of 22 studies were included. The results of meta-analyses showed that, there was a significant difference about LPA level in cerebral infarction (CI) group vs. healthy control group (WMD=2.00, 95%CI 1.85 to 2.15), and in transient ischemia attach (TIA) group vs. healthy control group (WMD=2.48, 95%CI 2.18 to 2.78); and a difference was noted about 24 hours LPA level in CI group vs. healthy control group (WMD=2.40, 95%CI 1.81 to 2.99). Conclusions According to the included studies, the contents of LPA is higher in CIS than that in healthy control group. It would be helpful to measure LPA in the TIA period for intervention. However, more high quality trials are expected for further study, in order to prove the value of LPA as early warning index because of the heterogeneity and poor quality of the current included studies.
ObjectiveTo investigate the effect of inhibiting autotaxin (ATX)-lysophosphatidic acid (LPA) pathway on the cartilage of knee osteoarthritis in rats.MethodsPrimary chondrocytes within three generations of Sprague-Dawley rats (8 weeks old, male) were randomly divided into 6 groups, including blank control group, model group, 1 μmol/L PF-8380 group, 10 μmol/L PF-8380 group, 1 μmol/L Ki16425 group, and 10 μmol/L Ki16425 group. Except for the blank control group, the other groups were modeled with osteoarthritis using interleukin-1β (10 ng/mL, 24 h), and then the experimental groups, i.e., 1 μmol/L PF-8380 group, 10 μmol/L PF-8380 group, 1 μmol/L Ki16425 group, and 10 μmol/L Ki16425 group, were intervened with 1, 10 μmol/L PF-8380 (ATX inhibitor) and 1, 10 μmol/L Ki16425 (LPA receptor antagonist) for 24 h, respectively. immunocytochemistry staining was used to determine the expression of type Ⅱ collagen (Col Ⅱ) in cytoplasm, and Western Blot was used to determine the expression of ATX, LPA, and matrix metalloproteinase-13 (MMP-13) in chondrocytes.ResultsCompared with the blank control group, the average absorbance of Col Ⅱ in chondrocytes in the model group was significantly reduced (0.003 9±0.000 8 vs. 0.110 0± 0.009 0, P<0.05). The expression levels of ATX, LPA, and MMP-13 in chondrocytes in the model group, 1 μmol/L PF-8380 group, 10 μmol/L PF-8380 group, and 1 μmol/L Ki16425 group were significantly higher than those in the blank control group, while the expression levels of ATX, LPA, and MMP-13 in the 10 μmol/L Ki16425 group had no significant difference with those in the blank control group; the expression levels of ATX, LPA, and MMP-13 in the model group, 10 μmol/L PF-8380 group, and 1 μmol/L PF-8380 group decreased in order; the expression levels of ATX, LPA, and MMP-13 in the model group, 1 μmol/L Ki16425 group, and 10 μmol/L Ki16425 group decreased in order.ConclusionInhibiting ATX-LPA pathway may inhibit the up-regulation of MMP-13 levels in articular cartilage of osteoarthritis in rats to reduce the damage of cartilage.