Anti-Matrix Metalloproteinase 1 Catalytic Domain monoclonal antibody, clone 5H7B11

Atrophic scars that occur after surgical procedure or trauma are considered as a cosmetic problem for patients. Atrophic scarring results usually during wound healing with inadequate production of collagen and connective tissue. Factors that precipitate to the formation of depressed scars include: individual variations in wound healing, wound tension, tissue apposition, and scar contraction. To evaluate the safety and efficacy of PRP vs carboxytherapy in treatment of atrophic scars. This study included 40 patients with atrophic scars divided into two groups; group A including 20 patients received PRP injection, group B including 20 patients received CO(2)injection. They received the treatment every 4 weeks for four sessions and had follow up for 6 months after the end of treatment. Skin biopsies were taken before and after treatment to evaluate clinical results. There was statistically significant difference between both groups in treating atrophic scars, regarding clinical improvement and patients' satisfaction with better results in group B. Histopathological examination showed significant expression of MMP-1 in group B more than group A. Both methods were safe and effective with minimal side effects with better improvement in patients treated with carboxytherapy than those treated with PRP.

Clematichinenoside AR (AR), a major active ingredient extracted from traditional Chinese herb Clematis chinensis Osbeck, has been demonstrated to possess anti-inflammatory and immune-modulatory activities in the treatment of experimental rheumatoid arthritis (RA). The therapeutic potential of AR was supposed to be closely correlated to its ability against tumor necrosis factor-alpha (TNF-alpha). Therefore, we aimed to explore the protective effects of Clematichinenoside AR against inflammation and cytotoxicity induced by human TNF-alpha. AR treatment significantly decreased IL-6 and IL-8 secretion, and attenuated MMP-1 production in human RA-derived fibroblastlike synoviocyte MH7A cells stimulated by recombinant human TNF-alpha (rhTNF-alpha). AR might antagonize rhTNF alpha-induced responses in MH7A cells through inhibiting p38 and ERK MAPKs signal activation. In TNF-alpha-sensitive murine fibroblast L929 cells, AR treatment attenuated the proliferation inhibition ratio induced by rhTNF-alpha/ActD and antagonized rhTNF-alpha-induced cytotoxicity. The cellular and nuclear morphological alterations in apoptotic characteristics induced by rhTNF-alpha/ActD in L929 cells were observed to be attenuated by the pretreatment with AR under a phase-contrast and fluorescence microscopy, respectively. The Annexin V-FITC/PI double-staining assay was performed to confirm that AR pretreatment obviously decreased the cell death. The antagonistic effects of AR against rhTNF-alpha-induced cytotoxicity might be potentially attributed to the degeneration of reactive oxygen species and the increasing of mitochondrial membrane potential, along with the suppression of durative phosphorylation of c-Jun N-terminal kinase (JNK). Collectively, our results indicated that AR antagonizes the inflammatory and cytotoxic activities induced by human TNF-alpha effectively in vitro, which provided further evidence for a novel mechanism underlying AR for treating RA correlating with excessive TNF-alpha production.