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Upregulation of cystathionine β-synthetase in the arcuate nucleus produces pain hypersensitivity via PKC upregulation and Glu N2B phosphorylation in rats with chronic pancreatitis
Pages: 575-584
Year: Issue:  5
Journal: Acta Physiologica Sinica

Keyword:  arcuate nucleuschronic pancreatitisabdominal painhydrogen sulfideNMDA receptorprotein kinase C;
Abstract: Hydrogen sulfide(H2S) contributes to visceral hyperalgesia in primary sensory neurons, but its role in central nervous system remains largely unknown. This study was to investigate the roles and underlying mechanisms of H2 S and its endogenous synthesis enzymes in the arcuate nucleus(ARC) in rat pancreatic hyperalgesia. Chronic pancreatitis(CP) was induced in male adult Sprague-Dawley rats by intra-pancreatic ductal injection of trinitrobenzene sulfonic acid(TNBS). Abdominal hyperalgesia was assessed by referred somatic behaviors to mechanical stimulation of rat abdomen. Western blot analysis was performed to detect protein expression in the ARC. CP markedly upregulated cystathionine β-synthetase(CBS) expression but did not alter cystathionine-γ-lyase level in the ARC at 4 weeks after TNBS injection. Although the expression of total Glu N2 B was not altered, CP greatly enhanced the phosphorylation level of Glu N2 B in the ARC when compared with age- and sex-matched control rats. CP also significantly increased expression of protein kinase Cγ(PKCγ) in the ARC. Arcuate microinjection of O-(Carboxymethyl) hydroxylamine hemihydrochloride(AOAA, an inhibitor of CBS) significantly attenuated abdominal pain in CP rats in a dose-dependent manner and reversed the CP-induced upregulation of p-Glu N2 B and PKCγ in the ARC. Furthermore, the Glu N2 B inhibitor or specific PKC inhibitor chelerythrine significantly attenuated abdominal hyperalgesia in CP rats. The p-Glu N2 B expression was also suppressed by PKC inhibitor. Taken together, our results suggest that the upregulation of CBS in the ARC leads to an activation of Glu N2 B via PKCγ, which may play an important role in generation of pain hypersensitivity of CP.
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