Alsabaani Nasser A, Osman Osama M, Dallak Mohamed A, Morsy Mohamed D, Al-Dhibi Hassan A
Department of Ophthalmology, College of Medicine, King Khalid University, Abha, Saudi Arabia.
Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia.
J Ophthalmol. 2022 Feb 28;2022:3044202. doi: 10.1155/2022/3044202. eCollection 2022.
This study tested the protective effect of maslinic acid (MA) against diabetic retinopathy (DR) in rats with type 1 diabetes mellitus (T1DM) and investigated possible mechanisms of action. DM was introduced by streptozotocin (STZ) (65 mg/kg, i.p.). Control and STZ (T1DM) were divided into 2 subgroups, which received either the vehicle or MA (80 mg/kg). Serum, pancreases, and retinas were collected for further use. MA significantly reduced fasting glucose levels in the control and T1DM rats but enhanced fasting insulin levels and partially increased the size of the islets of Langerhans and the number of -cells in T1DM rats. In addition, MA significantly improved the retina structure by preventing the reduction in the area between the inner and outer limiting membranes (ILM and OLM, respectively) and increasing the number of cells forming the ganglion cell layer (GCL), inner nuclear layer (INL), and outer nuclear layer (ONL). Associated with these effects, MA significantly reduced the total levels of tumor necrosis factor- (TNF-) and interleukin-6 (IL-6), as well as the nuclear levels of NF-B p65, mRNA levels of Bax, and protein levels of cleaved caspase-3 in the retinas of T1DM rats. However, MA significantly lowered levels of reactive oxygen species (ROS) and malondialdehyde (MDA) but significantly increased the nuclear levels of Nrf2, protein levels of Bcl2, and total levels of superoxide dismutase (SOD) and reduced glutathione (GSH) in the retinas of the control and T1DM rats. In conclusion, MA prevents DR by antioxidant potential mediated by the activation of Nrf2.
本研究测试了山楂酸(MA)对1型糖尿病(T1DM)大鼠糖尿病视网膜病变(DR)的保护作用,并研究了其可能的作用机制。通过腹腔注射链脲佐菌素(STZ)(65mg/kg)诱导糖尿病。将对照组和STZ诱导的T1DM组大鼠分为2个亚组,分别给予溶剂或MA(80mg/kg)。收集血清、胰腺和视网膜以供进一步研究。MA显著降低了对照组和T1DM大鼠的空腹血糖水平,但提高了空腹胰岛素水平,并部分增加了T1DM大鼠胰岛的大小和β细胞数量。此外,MA通过防止内、外限制膜(分别为ILM和OLM)之间面积的减少以及增加构成神经节细胞层(GCL)、内核层(INL)和外核层(ONL)的细胞数量,显著改善了视网膜结构。与这些作用相关,MA显著降低了T1DM大鼠视网膜中肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的总水平,以及NF-κB p65的核水平、Bax的mRNA水平和裂解的半胱天冬酶-3的蛋白水平。然而,MA显著降低了对照组和T1DM大鼠视网膜中活性氧(ROS)和丙二醛(MDA)的水平,但显著提高了Nrf2的核水平、Bcl2的蛋白水平以及超氧化物歧化酶(SOD)和还原型谷胱甘肽(GSH)的总水平。总之,MA通过激活Nrf2介导的抗氧化潜力预防DR。