Objectives This study aimed to assess the immunomodulatory effect of curcumin on innate and adaptive immune responses, as well as its inhibitory power on hyperglycemia in streptozotocin (STZ)-induced diabetic CD1 mice. Material and methods Mice were divided into six groups as follows: normal control mice (I), mice were intraperitoneally (i.p.) injected with either citrate (II), DEMSO (III), or curcumin (170 mg/kg, 3 times/week, for 28 days) (IV), as well as a single intraperitoneal injection of STZ (160 mg/kg) (V) and STZ mice treated with curcumin (VI). The anti-diabetic effect was assessed by estimation of the blood glucose concentration on days 3, 10, 17, 24, and 31. Differential count of white blood cells and the levels of cytokines were also measured at all previous time points. Pancreatic islets were examined for histopathological changes, and the immunohistochemical analysis for insulin and phosphorylated-nuclear factor-kappa B (phospho-NF-κB) was done at the end of the study. Results After curcumin administration, hyperglycemia was improved compared to diabetic mice; however, glucose concentration remains above the normal level. Treatment with curcumin selectively increased the count of lymphocytes and monocytes but decreased the granulocyte count in STZ diabetic mice. Diabetic mice treated with curcumin showed lower levels of interferon (IFN)-γ, interleukin (IL)-6, and IL-1β, as well as a higher level of IL-2 than in diabetic mice. Histopathological alterations that accompanied diabetes induction were ameliorated after curcumin administration. The pancreatic islets of treated diabetic mice displayed a decline in the immunostaining positivity of phospho-NF-κB compared to diabetic mice. Conclusion These results suggest that curcumin has anti-diabetic properties as it can improve the damage caused to the pancreatic β cells by its preferential immunomodulatory action on T helper1-related cytokines, as well as the immunosuppressive activity on proinflammatory cytokines.

中文翻译：

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姜黄素在链脲佐菌素诱导的糖尿病小鼠中诱导 β 细胞再生和磷酸化 NF-κB 的抑制

目的 本研究旨在评估姜黄素对先天性和适应性免疫反应的免疫调节作用，以及其对链脲佐菌素 (STZ) 诱导的糖尿病 CD1 小鼠高血糖的抑制能力。材料和方法将小鼠分为以下六组：正常对照小鼠（I），小鼠腹膜内（ip）注射柠檬酸盐（II）、DEMSO（III）或姜黄素（170 mg/kg，3次/周） ，持续 28 天）（IV），以及单次腹膜内注射 STZ（160 mg/kg）（V）和用姜黄素治疗的 STZ 小鼠（VI）。通过估计第 3、10、17、24 和 31 天的血糖浓度来评估抗糖尿病作用。还在所有之前的时间点测量白细胞的差异计数和细胞因子的水平。检查胰岛的组织病理学变化，在研究结束时对胰岛素和磷酸化核因子-κB (phospho-NF-κB) 进行免疫组织化学分析。结果姜黄素给药后，与糖尿病小鼠相比，高血糖得到改善；然而，葡萄糖浓度仍高于正常水平。姜黄素治疗选择性地增加了 STZ 糖尿病小鼠的淋巴细胞和单核细胞计数，但降低了粒细胞计数。与糖尿病小鼠相比，用姜黄素治疗的糖尿病小鼠的干扰素 (IFN)-γ、白细胞介素 (IL)-6 和 IL-1β 水平较低，IL-2 水平较高。姜黄素给药后伴随糖尿病诱导的组织病理学改变得到改善。与糖尿病小鼠相比，经治疗的糖尿病小鼠的胰岛显示磷酸化 NF-κB 的免疫染色阳性下降。结论 这些结果表明姜黄素具有抗糖尿病特性，因为它可以通过其对 T helper1 相关细胞因子的优先免疫调节作用以及对促炎细胞因子的免疫抑制活性来改善对胰腺 β 细胞造成的损伤。