Panminerva medica · 2020
Pranoprofen inhibits endoplasmic reticulum stress-mediated apoptosis of chondrocytes.
СтатьяНазвание и аннотация: Перевод в очереди
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Gong Yuqing, Zhang Wanqiang, Yan Peipei, Mu Yanping
Аннотация
BACKGROUND: Endoplasmic reticulum stress (ERS) is a newly discovered pathway that causes apoptosis. At present, there is little research about the non-steroidal anti-inflammatory drug (NSAID) on the apoptosis of chondrocytes CHs. Our study aimed to test the anti-apoptosis effects of pranoprofen (PF), a specific prostaglandin E2 (PGE2) inhibitor, on human CHs.
METHODS: We firstly made a distinguish about the levels of PGE2, ERS, and apoptosis between cartilage with and without OA. Then CHs isolated from healthy cartilage were pretreated H<inf>2</inf>O<inf>2</inf> or tunicamycin (TM) to activate ERS, and then exposed to PF. Expression of type II collagen, Runx-2, COX-9, SOD1, GPX1, GRP78, CHOP, caspase-12, ROS level, and apoptosis cell ratio was determined by immunofluorescence, Western blot, RT-PCR, or flow cytometry respectively.
RESULTS: We found that oxidative stress, PGE2, ERS, and apoptosis were upregulated in OA cartilage. In addition, H<inf>2</inf>O<inf>2</inf> and TM could increase the levels of PGE2, GRP78, CHOP, caspase-12, and reactive oxygen species (ROS), resulting in the degeneration of CHs. PF significantly reduced the expression of PGE2 and suppressed the ERS and apoptosis caused by H<inf>2</inf>O<inf>2</inf> and TM, showing a protective function of CHs degeneration.
CONCLUSIONS: This study demonstrates the anti-apoptotic effect of PF in the abrogation of the ERS-mediated apoptosis in human CHs, suggesting a new mechanism of PF in the treatment of OA.
METHODS: We firstly made a distinguish about the levels of PGE2, ERS, and apoptosis between cartilage with and without OA. Then CHs isolated from healthy cartilage were pretreated H<inf>2</inf>O<inf>2</inf> or tunicamycin (TM) to activate ERS, and then exposed to PF. Expression of type II collagen, Runx-2, COX-9, SOD1, GPX1, GRP78, CHOP, caspase-12, ROS level, and apoptosis cell ratio was determined by immunofluorescence, Western blot, RT-PCR, or flow cytometry respectively.
RESULTS: We found that oxidative stress, PGE2, ERS, and apoptosis were upregulated in OA cartilage. In addition, H<inf>2</inf>O<inf>2</inf> and TM could increase the levels of PGE2, GRP78, CHOP, caspase-12, and reactive oxygen species (ROS), resulting in the degeneration of CHs. PF significantly reduced the expression of PGE2 and suppressed the ERS and apoptosis caused by H<inf>2</inf>O<inf>2</inf> and TM, showing a protective function of CHs degeneration.
CONCLUSIONS: This study demonstrates the anti-apoptotic effect of PF in the abrogation of the ERS-mediated apoptosis in human CHs, suggesting a new mechanism of PF in the treatment of OA.