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Vascular endothelial growth factor (VEGF) is expressed in articular cartilage and increases in expression levels have been associated with the progression of osteoarthritis (OA). Thalidomide is a drug that has been reported to inhibit angiogenesis and reduce VEGF production by downregulating VEGF expression. The objective of the present study was to determine whether intraperitoneal administration of thalidomide may attenuate early OA development in mice. Male C57BL/6 mice (10‑weeks‑old) were randomly assigned into the destabilization of the medial meniscus (Dmm) with thalidomide treatment (Dmm+Th), Dmm and Sham groups equally. An OA model was induced surgically in Dmm+Th and Dmm groups, and mice of the Dmm+Th group were subsequently treated with an intraperitoneal injection of thalidomide (200 mg/kg/day). At 2 and 4 weeks following surgery, the pathological alterations in cartilage samples were assessed qualitatively by hematoxylin and eosin staining and Safranin O/Fast green staining, and quantitatively by the Osteoarthritis Research Society International scoring system. The mRNA expression levels of matrix metalloproteinase‑13 (MMP‑13) and VEGF were measured by reverse transcription‑quantitative polymerase chain reaction. The protein expression levels of MMP‑13 and VEGF were detected by immunofluorescence and immunohistochemistry, respectively. The production of VEGF in serum was evaluated via an ELISA assay. Pathological scores were significantly higher in the Dmm and the Dmm+Th groups than those in the Sham group; however, the Dmm+Th group exhibited markedly less severe pathological changes compared with the Dmm group. Compared with the Sham group, the mRNA and protein expression levels of VEGF and MMP‑13 in the Dmm and the Dmm+Th groups were significantly increased. The Dmm+Th group exhibited significantly decreased expression levels of VEGF and MMP‑13, as well as significantly decreased serum VEGF concentration compared with the Dmm group. Thus, the results of the present study demonstrated that intraperitoneal administration of thalidomide may alleviate the development of early OA by suppressing VEGF expression in mice and may have potential as a novel therapy for the treatment of OA.

To determine the effect of tanshinone II A on the transmembrance action potential of three layers of myocardial cells in LQT2 rabbit models.Whole-cell patch clamp technique was used to record the action potential duration 90 (APD90) and the transmural dispersion of repolarization (TDR) of the epicardium, mid-myocardium and endocardium in the LQT2 rabbits.Of the three layers of myocardial cells, the mid-myocardium had the longest APD90 and the epicardium had the shortest APD90. The APD90 of all three layers of myocardial cells were shortened with infusion of 10 mg/mL tanshinone II A. Their TDR values also reduced by the infusion.Tanshinone II A shortens APD90 and reduces TDR values.