Physiology Department, Faculty of Medicine, Minia University, Minia, 61111, Egypt.
Histology and Cell Biology Department, Faculty of Medicine, Minia University, Minia, 61111, Egypt.
Cell Stress Chaperones. 2019 May;24(3):567-580. doi: 10.1007/s12192-019-00988-y. Epub 2019 Mar 22.
Chronic stress has been linked to many diseases resulted from dysfunction of both the nervous system and peripheral organ systems. Yet, the effects of chronic stress on the pancreas have received relatively little attention. This work aims to investigate the influence of chronic stress exposure on both the endocrine and exocrine pancreatic function and morphology and its possible mechanism of action, and also to evaluate the impact of chronic exercise with moderate intensity on ameliorating the stress-induced pancreatic changes. Forty adult male albino rats were used and divided into four groups: control group, exercised group (3 weeks of swimming exercise), stressed group (3 weeks of immobilization stress), and stressed group practicing exercise (3 weeks of exercise, concomitant with 21 daily sessions of stress). On the final day of the experiment, all rats were sacrificed. Biochemical, immunohistochemical, and histological studies were conducted. The results showed that chronic immobilization stress produced hyperglycemia, hyperinsulinemia, and increased homeostatic model assessment of insulin resistance index (HOMA-IR) with increasing exocrine pancreatic injury markers by increasing oxidative and inflammatory status of the pancreatic tissue. Histological study showed the injurious effect of stress on the morphology of pancreatic tissue. Physical exercise protected the pancreas from the negative effects of stress through its anti-inflammatory and anti-oxidative effects, evidenced by increasing pancreatic interleukin 10 and total antioxidant capacity and decreasing pancreatic tumor necrosis factor-alpha, and malondialdehyde with ameliorating most of the histological changes induced by stress exposure. Physical exercise effectively counteracts chronic stress-induced pancreatic changes through different mechanisms.
慢性应激与神经系统和外周器官系统功能障碍引起的许多疾病有关。然而,慢性应激对胰腺的影响相对较少受到关注。本研究旨在探讨慢性应激暴露对胰腺内分泌和外分泌功能和形态的影响及其可能的作用机制,并评估中等强度慢性运动对改善应激诱导的胰腺变化的影响。使用 40 只成年雄性白化大鼠,并将其分为四组:对照组、运动组(3 周游泳运动)、应激组(3 周固定应激)和运动应激组(3 周运动,同时进行 21 次每日应激)。在实验的最后一天,所有大鼠均被处死。进行了生化、免疫组织化学和组织学研究。结果表明,慢性固定应激导致高血糖、高胰岛素血症和稳态模型评估的胰岛素抵抗指数(HOMA-IR)升高,同时通过增加胰腺组织的氧化和炎症状态,增加了外分泌胰腺损伤标志物。组织学研究显示应激对胰腺组织形态有损伤作用。运动通过其抗炎和抗氧化作用保护胰腺免受应激的负面影响,表现为增加胰腺白细胞介素 10 和总抗氧化能力,降低胰腺肿瘤坏死因子-α和丙二醛,改善应激暴露引起的大多数组织学变化。运动通过不同的机制有效对抗慢性应激引起的胰腺变化。