Acute pancreatitis (AP) is a sudden pancreatic inflammation accompanied by an excessive reactive oxygen species production that provokes inflammation. The present study investigated whether carvedilol can protect against l-arginine induced AP in a rat model and studied the mechanisms associated with its protection.

Rats were divided into four groups: a control group, an AP group (injected with 2 doses of l-arginine 250 mg/100 g body weight at 1 h interval, intraperitoneally) on the 22nd day of the experiment, a carvedilol group (10 mg/kg, orally) for 21 successive days, and finally a carvedilol + AP group. It was found that pretreatment with carvedilol decreased α-amylase and lipase activities as well as C-reactive protein (CRP) and malondialdehyde levels; on the other hand, it improved the reduced glutathione (GSH) level and catalase (CAT) activity. In addition, carvedilol markedly decreased all of the following biomarkers: nuclear factor kappa B (NF-κB p65), p38 mitogen-activated protein kinases (P38-MAPK), signal transducer and activator of transcription 1 (STAT1-α), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), myeloperoxidase (MPO), and phospholipase A2 (PLA2) levels that was induced by l-arginine. Finally, carvedilol noticeably down regulated the pancreatitis associated protein (PAP2) and the pancreas platelets activating factor (PAF) genes expression.

In conclusion: carvedilol protected against l-arginine induced AP in rats, via the inhibition of cellular oxidative stress and inflammatory pathways that contributed to pancreas injury.

急性胰腺炎（AP）是一种突然的胰腺炎症，并伴有过多的活性氧产生，从而引起炎症。本研究调查了卡维地洛是否可以预防l-精氨酸诱导的AP在大鼠模型中，并研究了与之相关的保护机制。

将大鼠分为四组：对照组，AP组（每隔1 h注射2剂量的1-精氨酸250 mg / 100 g体重，腹膜内注射））在实验的第22天，连续21天使用卡维地洛组（口服10 mg / kg），最后使用卡维地洛+ AP组。发现卡维地洛预处理可降低α-淀粉酶和脂肪酶活性以及C反应蛋白（CRP）和丙二醛水平。另一方面，它改善了降低的谷胱甘肽（GSH）水平和过氧化氢酶（CAT）活性。此外，卡维地洛显着降低了以下所有生物标志物：核因子κB（NF-κBp65），p38丝裂原活化蛋白激酶（P38-MAPK），信号转导和转录激活因子1（STAT1-α），肿瘤坏死l诱导的因子-α（TNF-α），白介素-1β（IL-1β），髓过氧化物酶（MPO）和磷脂酶A2（PLA2）水平-精氨酸 最后，卡维地洛显着下调了胰腺炎相关蛋白（PAP2）和胰腺血小板活化因子（PAF）基因的表达。

结论：卡维地洛可通过抑制细胞氧化应激和炎症途径来保护胰腺免受l-精氨酸诱导的AP的侵害。