Octreotide alleviates pancreatic damage caused by paraquat in rats by reducing inflammatory responses and oxidative stress

•Paraquat can cause pancreatic injury.•Octreotide could mitigate paraquat-induced systemic inflammatory response.•Octreotide can antagonize the pancreatic injury via NF-κB signaling pathway. This study explores the efficacy and mechanism by which octreotide (OCT) alleviates paraquat (PQ)-induced pan...

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Veröffentlicht in:Environmental toxicology and pharmacology 2020-11, Vol.80, p.103456, Article 103456
Hauptverfasser: Gao, Yanxia, Hou, Linlin, Wang, Yibo, Guo, Shigong, Yuan, Ding, Jiang, Ya’nan, Duan, Guoyu, Zhang, Yan, Xu, Zhigao, Che, Lu, Sun, Changhua, Li, Sujuan, Zhang, Shoutao, Sun, Tongwen, Li, Yi
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Sprache:eng
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Zusammenfassung:•Paraquat can cause pancreatic injury.•Octreotide could mitigate paraquat-induced systemic inflammatory response.•Octreotide can antagonize the pancreatic injury via NF-κB signaling pathway. This study explores the efficacy and mechanism by which octreotide (OCT) alleviates paraquat (PQ)-induced pancreatic injury. Twenty-four adult male rats were randomly divided into three groups: the normal control (NC), PQ poisoning, and OCT treatment groups. The PQ-induced pancreatic injury rat model was established by administering PQ (120 mg/kg). Treatment group rats received OCT (8 μg/kg body weight) every 8 h by subcutaneous injection, 1 h after PQ administration. Rats were euthanized 24 h after PQ injection. Serum amylase, lipase, tumor necrosis factor-α, and interleukin-6 levels were markedly increased in the PQ group versus the NC group. In pancreatic tissue, PQ poisoning drastically induced necrosis and increased inflammatory cytokine and oxidative stress marker levels. Compared with the PQ group, OCT reduced pancreatic damage and histological scores, serum amylase, lipase, and inflammatory cytokine levels, as well as oxidative stress. OCT demonstrates protective effects against PQ-induced pancreatic damage through anti-inflammatory and antioxidant actions.
ISSN:1382-6689
1872-7077
DOI:10.1016/j.etap.2020.103456