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CB2 receptor activation ameliorates the proinflammatory activity in acute lung
injury induced by paraquat
#MMPMID24963491
Liu Z
; Wang Y
; Zhao H
; Zheng Q
; Xiao L
; Zhao M
Biomed Res Int
2014[]; 2014
(?): 971750
PMID24963491
show ga
Paraquat, a widely used herbicide, is well known to exhibit oxidative stress and
lung injury. In the present study, we investigated the possible underlying
mechanisms of cannabinoid receptor-2 (CB2) activation to ameliorate the
proinflammatory activity induced by PQ in rats. JWH133, a CB2 agonist, was
administered by intraperitoneal injection 1 h prior to PQ exposure. After PQ
exposure for 4, 8, 24, and 72 h, the bronchoalveolar lavage fluid was collected
to determine levels of TNF-? and IL-1?, and the arterial blood samples were
collected for detection of PaO2 level. At 72 h after PQ exposure, lung tissues
were collected to determine the lung wet-to-dry weight ratios, myeloperoxidase
activity, lung histopathology, the protein expression level of CB2, MAPKs
(ERK1/2, p38MAPK, and JNK1/2), and NF-?Bp65. After rats were pretreated with
JWH133, PQ-induced lung edema and lung histopathological changes were
significantly attenuated. PQ-induced TNF-? and IL-1? secretion in BALF, increases
of PaO2 in arterial blood, and MPO levels in the lung tissue were significantly
reduced. JWH133 could efficiently activate CB2, while inhibiting MAPKs and NF-?B
activation. The results suggested that activating CB2 receptor exerted protective
activity against PQ-induced ALI, and it potentially contributed to the
suppression of the activation of MAPKs and NF-?B pathways.
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