Paraquat, a widely used herbicide, is well known to exhibit oxidative stress and lung injury. In the present study, we investigated the\npossible underlying mechanisms of cannabinoid receptor-2 (CB2) activation to ameliorate the proinflammatory activity induced by\nPQ in rats. JWH133, a CB2 agonist, was administered by intraperitoneal injection 1 h prior to PQ exposure. After PQ exposure for 4,\n8, 24, and 72 h, the bronchoalveolar lavage fluid was collected to determine levels of TNF-???? and IL-1????, and the arterial blood samples\nwere collected for detection of PaO2 level. At 72 h after PQ exposure, lung tissues were collected to determine the lung wet-to-dry\nweight ratios,myeloperoxidase activity, lung histopathology, the protein expression level of CB2, MAPKs (ERK1/2, p38MAPK, and\nJNK1/2), andNF-????Bp65. After rats were pretreated with JWH133, PQ-induced lung edema and lung histopathological changes were\nsignificantly attenuated. PQ-induced TNF-???? and IL-1???? secretion in BALF, increases of PaO2 in arterial blood, andMPOlevels in the\nlung tissue were significantly reduced. JWH133 could efficiently activate CB2, while inhibiting MAPKs and NF-????B activation. The\nresults suggested that activating CB2 receptor exerted protective activity against PQ-induced ALI, and it potentially contributed to\nthe suppression of the activation of MAPKs and NF-????B pathways.
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