Human MMP-1(Matrix Metalloproteinase 1) ELISA Kit

Anterior cruciate ligament (ACL) injury is one of the common injuries in sports and vehicle accidents. ACL decreases joint stability, leading to increased incidence of osteoarthritis. Although there are various approaches for the reconstruction of ACL, no consensus has been reached on the safest and most effective method to achieve joint stability. Here we have compared the biomechanical and histopathological outcomes of three different approaches: intra-articular ACL reconstruction, remnant-preserving and re-tensioning and non-remnant-preservation technique, using finite element analysis, histopathologic observation as well as qPCR and western blot analysis. Results of the current study showed no significant differences among the three methods concerning biomechanical, histopathological analysis and mRNA and protein levels of chondrocyte apoptotic markers such as JNK, MMP-1 and SIRT1 (P > 0.05). Those results indicated that remnant preservation techniques such as intra-articular ACL reconstruction and remnant-preserving and re-tensioning are similar in their ability to achieve joint stabilization and prevent chondrocyte regeneration to non-remnant-preservation technique.

Tendinopathy is a rare but serious complication of quinolone therapy. Risk factors associated with quinolone-induced tendon disorders include chronic kidney disease accompanied by the accumulation of uremic toxins. Hence, the present study explored the effects of the representative uremic toxins phenylacetic acid (PAA) and quinolinic acid (QA), both alone and in combination with ciprofloxacin (CPX), on human tenocytes in vitro. Tenocytes incubated with uremic toxins +/- CPX were investigated for metabolic activity, vitality, expression of the dominant extracellular tendon matrix (ECM) protein type I collagen, cell-matrix receptor beta 1-integrin, proinflammatory interleukin (IL)-1 beta, and the ECM-degrading enzyme matrix metalloproteinase (MMP)-1. CPX, when administered at high concentrations (100 mM), suppressed tenocyte metabolism after 8 h exposure and at therapeutic concentrations after 72 h exposure. PAA reduced tenocyte metabolism only after 72 h exposure to very high doses and when combined with CPX. QA, when administered alone, led to scarcely any cytotoxic effect. Combinations of CPX with PAA or QA did not cause greater cytotoxicity than incubation with CPX alone. Gene expression of the pro-inflammatory cytokine IL-1 beta was reduced by CPX but up-regulated by PAA and QA. Protein levels of type I collagen decreased in response to high CPX doses, whereas PAA and QA did not affect its synthesis significantly. MMP-1 mRNA levels were increased by CPX. This effect became more pronounced in the form of a synergism following exposure to a combination of CPX and PAA. CPX was more tenotoxic than the uremic toxins PAA and QA, which showed only distinct suppressive effects.