title: Millimeter wave treatment inhibits NO-induced apoptosis of chondrocytes through the p38MAPK pathway.
abstract: In the present study, we investigated the effects of millimeter wave treatment on the activation of the p38MAPK signaling pathway in the process of NO-induced apoptosis in chondrocytes. Cartilage was isolated from the knee joint of SD rats and used to establish cultured primary chondrocytes. After identification using in situ staining of type II collagen, the passage 2 chondrocytes were incubated with or without sodium nitroprussiate (SNP) to induce apoptosis and treated with a millimeter wave for various times. The apoptosis of chondrocytes was detected using immunofluorescence, an MTT assay, and Annexin V-FITC labeling followed by fluorescence-activated cell sorting (FACS). The activity of caspase-3 was measured using colorimeters, and the levels of p38 and p53 were also detected using RT-PCR and Western blotting. After treatment with SNP, the OD values of the experimental groups were significantly lower than the control group (P<0.01). The 24-h interference of a millimeter wave significantly prevented apoptosis (P<0.01) and showed a dose dependency, and an identical trend of apoptosis was noted with normal cell number counting (P<0.01) and FACS (P<0.01). Consistently, the caspase 3 activity showed a reverse trend, with the highest activity in the experimental group receiving no millimeter wave treatment (P<0.01). The mRNA expression of p38 and p53 and the protein levels of phosphorylated p38 and p53 showed a similar trend (P<0.01) to that of caspase 3 activity. In conclusion, millimeter wave treatment inhibits the SNP-induced apoptosis of chondrocytes through the p38MAPK pathway.
authors.affiliation: Huatuo, University Town, Minhou Shangjie, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350108, P.R. China.
authors.forename: Xihai
authors.initials: X
authors.lastname: Li
authors.forename: Min
authors.initials: M
authors.lastname: Du
authors.forename: Xianxiang
authors.initials: X
authors.lastname: Liu
authors.forename: Mingxia
authors.initials: M
authors.lastname: Wu
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Ye
authors.forename: Jiumao
authors.initials: J
authors.lastname: Lin
authors.forename: Wenlie
authors.initials: W
authors.lastname: Chen
authors.forename: Guangwen
authors.initials: G
authors.lastname: Wu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000528:radiation effects*; D002478:Cells, Cultured; D019902:Chondrocytes / Q000166:cytology / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects*; D004789:Enzyme Activation; D007719:Knee Joint / Q000033:anatomy & histology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D011827:Radiation; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects / Q000528:radiation effects*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D020030:Nitric Oxide Donors; D016159:Tumor Suppressor Protein p53; D009599:Nitroprusside; D009569:Nitric Oxide; D048051:p38 Mitogen-Activated Protein Kinases