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Abstract：
OBJECTIVE: It was aimed to investigate the biochemical and histopathological effects of resveratrol and melatonin, via histone H4 and β-defensin 1, in diabetic rats.
METHODS: Twenty-four Sprague-Dawley male rats were categorized into 4 groups, with 6 rats in each group (control, diabetes mellitus, melatonin - diabetes mellitus, and resveratrol+diabetes mellitus). Diabetes was formed by giving streptozotocin to all groups except the control group. Melatonin, 5 mg/kg/day, was given to the melatonin - diabetes mellitus group, and resveratrol, 5 mg/kg/day, was given to the resveratrol+diabetes mellitus group via intraperitoneally for 3 weeks. Interleukin-1 beta, tumor necrosis factor alpha, histone H4, and β-defensin 1 levels were measured in the blood of all rats. The lung, liver, and kidney tissue of all rats were performed as histopathological examinations.
RESULTS: Whereas there was no difference between the other groups (P >.05), interleukin-1 beta levels of the diabetes mellitus group were found to be significantly higher compared with the control group (5.02 ± 2.15 vs. 2.38 ± 0.72 ng/mL; P < .05). Whereas histone H4 levels of the diabetes mellitus group were higher compared with the control and resveratrol+diabetes mellitus groups (7.53 ± 3.30 vs. 2.97 ± 1.57 and 3.06 ± 1.57 ng/mL; P <.05), the β-defensin 1 levels of the diabetes mellitus group were lower compared with control and resveratrol+diabetes mellitus groups (7.6 ± 2.8 vs. 21.6 ± 5.5 and 18.8 ± 7.4 ng/mL; P <.05). β-Defensin 1 levels were moderately inversely correlated with interleukin-1 beta and histone H4 levels (rs > -0.50, P < .01). Histopathological changes found in favor of target cell damage in the diabetes mellitus group were not observed in resveratrol+diabetes mellitus group.
CONCLUSIONS: Resveratrol may be used as a biotherapeutic agent, which significantly reduces diabetes-induced histone H4 and interleukin-1 beta-mediated liver and other target organ damage.
METHODS: Twenty-four Sprague-Dawley male rats were categorized into 4 groups, with 6 rats in each group (control, diabetes mellitus, melatonin - diabetes mellitus, and resveratrol+diabetes mellitus). Diabetes was formed by giving streptozotocin to all groups except the control group. Melatonin, 5 mg/kg/day, was given to the melatonin - diabetes mellitus group, and resveratrol, 5 mg/kg/day, was given to the resveratrol+diabetes mellitus group via intraperitoneally for 3 weeks. Interleukin-1 beta, tumor necrosis factor alpha, histone H4, and β-defensin 1 levels were measured in the blood of all rats. The lung, liver, and kidney tissue of all rats were performed as histopathological examinations.
RESULTS: Whereas there was no difference between the other groups (P >.05), interleukin-1 beta levels of the diabetes mellitus group were found to be significantly higher compared with the control group (5.02 ± 2.15 vs. 2.38 ± 0.72 ng/mL; P < .05). Whereas histone H4 levels of the diabetes mellitus group were higher compared with the control and resveratrol+diabetes mellitus groups (7.53 ± 3.30 vs. 2.97 ± 1.57 and 3.06 ± 1.57 ng/mL; P <.05), the β-defensin 1 levels of the diabetes mellitus group were lower compared with control and resveratrol+diabetes mellitus groups (7.6 ± 2.8 vs. 21.6 ± 5.5 and 18.8 ± 7.4 ng/mL; P <.05). β-Defensin 1 levels were moderately inversely correlated with interleukin-1 beta and histone H4 levels (rs > -0.50, P < .01). Histopathological changes found in favor of target cell damage in the diabetes mellitus group were not observed in resveratrol+diabetes mellitus group.
CONCLUSIONS: Resveratrol may be used as a biotherapeutic agent, which significantly reduces diabetes-induced histone H4 and interleukin-1 beta-mediated liver and other target organ damage.
摘要：
目的：研究白藜芦醇和褪黑素的生化和组织病理学影响，通过组蛋白H4和β-防御素1，在糖尿病大鼠中。
方法：将24只Sprague-Dawley雄性大鼠分为4组，每组6只大鼠(对照组，糖尿病,褪黑素-糖尿病，和白藜芦醇+糖尿病)。糖尿病是通过向除对照组外的所有组给予链脲佐菌素而形成的。褪黑激素,5mg/kg/天，给褪黑激素-糖尿病组，和白藜芦醇,5mg/kg/天，白藜芦醇+糖尿病组经腹腔给药3周。白细胞介素-1β，肿瘤坏死因子α,在所有大鼠的血液中测量组蛋白H4和β-防御素1水平。肺，肝脏,对所有大鼠的肾组织进行组织病理学检查。
结果：而其他组之间没有差异（P>0.05），发现糖尿病组的白介素1β水平明显高于对照组（5.02±2.15vs.2.38±0.72ng/mL；P<.05）。而糖尿病组的组蛋白H4水平高于对照组和白藜芦醇+糖尿病组（7.53±3.30vs.2.97±1.57和3.06±1.57ng/mL；P<.05），与对照组和白藜芦醇+糖尿病组相比，糖尿病组的β-防御素1水平较低（7.6±2.8vs.21.6±5.5和18.8±7.4ng/mL；P<.05）。β-防御素1水平与白细胞介素-1β和组蛋白H4水平呈中度负相关（rs>-0.50，P<.01）。白藜芦醇+糖尿病组未观察到糖尿病组有利于靶细胞损伤的组织病理学变化。
结论：白藜芦醇可用作生物治疗剂，显着减少糖尿病诱导的组蛋白H4和白细胞介素-1β介导的肝脏和其他靶器官损伤。
方法：将24只Sprague-Dawley雄性大鼠分为4组，每组6只大鼠(对照组，糖尿病,褪黑素-糖尿病，和白藜芦醇+糖尿病)。糖尿病是通过向除对照组外的所有组给予链脲佐菌素而形成的。褪黑激素,5mg/kg/天，给褪黑激素-糖尿病组，和白藜芦醇,5mg/kg/天，白藜芦醇+糖尿病组经腹腔给药3周。白细胞介素-1β，肿瘤坏死因子α,在所有大鼠的血液中测量组蛋白H4和β-防御素1水平。肺，肝脏,对所有大鼠的肾组织进行组织病理学检查。
结果：而其他组之间没有差异（P>0.05），发现糖尿病组的白介素1β水平明显高于对照组（5.02±2.15vs.2.38±0.72ng/mL；P<.05）。而糖尿病组的组蛋白H4水平高于对照组和白藜芦醇+糖尿病组（7.53±3.30vs.2.97±1.57和3.06±1.57ng/mL；P<.05），与对照组和白藜芦醇+糖尿病组相比，糖尿病组的β-防御素1水平较低（7.6±2.8vs.21.6±5.5和18.8±7.4ng/mL；P<.05）。β-防御素1水平与白细胞介素-1β和组蛋白H4水平呈中度负相关（rs>-0.50，P<.01）。白藜芦醇+糖尿病组未观察到糖尿病组有利于靶细胞损伤的组织病理学变化。
结论：白藜芦醇可用作生物治疗剂，显着减少糖尿病诱导的组蛋白H4和白细胞介素-1β介导的肝脏和其他靶器官损伤。
