Department of Pulmonary and Critical Care Medicine, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, China
Department of Pulmonary and Critical Care Medicine, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, China.
BMJ Open Diabetes Res Care. 2023 Apr;11(2). doi: 10.1136/bmjdrc-2022-003027.
Diabetic lung disease is already known as one of the diabetes complications, but report on its therapeutic strategy is rare. The present study aimed to add novel therapeutic strategy for diabetic lung disease, to reveal the protective effect of ghrelin on diabetic lung disease both in vivo and in vitro, and to discuss its probable molecular mechanism.
Diabetic mice and 16HBE cells were our research objects. We surveyed the effect of ghrelin on streptozotocin-induced lung tissue morphology changes by H&E staining. Furthermore, the changes of proinflammatory cytokines (interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)) were detected by ELISA. To expound the molecular mechanism, we detected critical proteins of TLR4 pathway and observed their changes by immunohistochemistry (IHC), real-time PCR and western blot analysis in vivo and in vitro, respectively.
The results of H&E staining showed that pathological alterations of the lung induced by hyperglycemia were ameliorated by ghrelin. The results of ELISA demonstrated that the elevated levels of IL-1β and TNF-α induced by hyperglycemia turned to decrease in the lung after ghrelin treatment. In the results of IHC, real-time PCR and western blot analysis, we found that the TLR4 pathway was elevated by hyperglycemia or high glucose and is remarkably inhibited by the treatment of ghrelin both in vivo and in vitro.
Ghrelin could inhibit inflammation of diabetic lung disease by regulating the TLR4 pathway. This study might affect research on diabetic lung disease, and the therapeutic potential of ghrelin for diabetic lung disease is worth considering.
糖尿病肺部疾病已被认为是糖尿病并发症之一，但关于其治疗策略的报道却很少。本研究旨在为糖尿病肺部疾病添加新的治疗策略，揭示胃饥饿素对糖尿病肺部疾病的体内和体外保护作用，并探讨其可能的分子机制。
以糖尿病小鼠和 16HBE 细胞为研究对象。我们通过 H&E 染色观察胃饥饿素对链脲佐菌素诱导的肺组织形态变化的影响。此外，通过 ELISA 检测促炎细胞因子（白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α））的变化。为了阐述分子机制，我们通过免疫组化（IHC）、实时 PCR 和 Western blot 分析分别检测了 TLR4 通路的关键蛋白，并观察了它们在体内和体外的变化。
H&E 染色结果表明，高血糖引起的肺组织病理改变被胃饥饿素改善。ELISA 结果表明，高血糖诱导的 IL-1β和 TNF-α水平升高，经胃饥饿素治疗后降低。在 IHC、实时 PCR 和 Western blot 分析结果中，我们发现 TLR4 通路在高血糖或高糖条件下被激活，而在体内和体外，胃饥饿素治疗均显著抑制该通路。
胃饥饿素可通过调节 TLR4 通路抑制糖尿病肺部疾病的炎症。本研究可能会影响对糖尿病肺部疾病的研究，胃饥饿素治疗糖尿病肺部疾病的治疗潜力值得考虑。
