AIM To study the effects of sera derived from rats administrated Lugu Ganoderma Lucidum (LGL) on the expression of adhesion molecules ICAM 1 and VCAM 1 induced by oxidative low density lipoprotein (ox LDL) and glycated albumin METHODS The expression of ICAM 1 and VCAM 1 on the surface of endothelial cells was detected by endothelial cell enzyme linked immunosobent assay (ELISA) and flow cytometric technique RESULTS The results by cell ELISA demonstrated that the sera derived from the rats administrated 0 12 g?kg -1 p o of LGL did not show significant effects on theexpression of ICAM 1 induced by ox LDL, but the sera from the rats administrated 0 24 g?kg -1 , 0 72 g?kg -1 po for ten days produced significant effects of inhibiting the expression of ICAM 1 induced by ox LDL and the expression of ICAM 1 and VCAM 1 induced by glycated albumin The results by flow cytometric techniques showed that the sera from the rats administrated 0 72 g?kg -1 for ten days produced the same effect on ICAM 1 induced by ox LDL and glycated albumin CONCLUSION Lugu Ganoderma Lucidum can inhibit the expression of adhesion molecules on the surface of endothelial cells induced by ox LDL and glycated albumin.

AIM To establish an efficient and convenient system for expressing functional proteins. METHODS Xenopus leavis females were injected with HCG, eggs were harvested next morning and dejellied by 2% cysteine, from which the Xenopus leavis egg cell free translating system was prepared. Through subcloning technique, TFAR19 gene was cloned to pBluescript SK plasmid which was linearized by enzyme, then transcript and capped in vitro to synthesis the cRNA of TFAR19. RESULTS This cRNA was translated in freshly prepared cell free translating system, the product was identified by Western Blot. CONCLUSION The results showed that this translating system could efficiently translate TFAR19 cRNA and be a very useful translating tool.

The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint (TMJ) osteoarthritis (OA); however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4 (Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2 and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore, Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis.
Aggrecans/metabolism* ; Animals ; Cartilage, Articular/metabolism* ; Chondrocytes/pathology* ; Cytoskeletal Proteins/metabolism* ; Mice ; Muscle Proteins/metabolism* ; Osteoarthritis/pathology* ; Temporomandibular Joint/pathology*