PDF(Pubmed)
Abstract：
UNASSIGNED: Diabetes is closely linked to hearing loss, yet the exact mechanisms remain unclear. Cochlear stria vascularis and pericytes (PCs) are crucial for hearing. This study investigates whether high glucose induces apoptosis in the cochlear stria vascularis and pericytes via elevated ROS levels due to oxidative stress, impacting hearing loss.
UNASSIGNED: We established a type II diabetes model in C57BL/6J mice and used auditory brainstem response (ABR), Evans blue staining, HE staining, immunohistochemistry, and immunofluorescence to observe changes in hearing, blood-labyrinth barrier (BLB) permeability, stria vascularis morphology, and apoptosis protein expression. Primary cultured stria vascularis pericytes were subjected to high glucose, and apoptosis levels were assessed using flow cytometry, Annexin V-FITC, Hoechst 33342 staining, Western blot, Mitosox, and JC-1 probes.
UNASSIGNED: Diabetic mice showed decreased hearing thresholds, reduced stria vascularis density, increased oxidative stress, cell apoptosis, and decreased antioxidant levels. High glucose exposure increased apoptosis and ROS content in pericytes, while mitochondrial membrane potential decreased, with AIF and cytochrome C (CytC) released from mitochondria to the cytoplasm. Adding oxidative scavengers reduced AIF and CytC release, decreasing pericyte apoptosis.
UNASSIGNED: Hyperglycemia may induce mitochondrial apoptosis of cochlear stria vascularis pericytes through oxidative stress.
UNASSIGNED: We established a type II diabetes model in C57BL/6J mice and used auditory brainstem response (ABR), Evans blue staining, HE staining, immunohistochemistry, and immunofluorescence to observe changes in hearing, blood-labyrinth barrier (BLB) permeability, stria vascularis morphology, and apoptosis protein expression. Primary cultured stria vascularis pericytes were subjected to high glucose, and apoptosis levels were assessed using flow cytometry, Annexin V-FITC, Hoechst 33342 staining, Western blot, Mitosox, and JC-1 probes.
UNASSIGNED: Diabetic mice showed decreased hearing thresholds, reduced stria vascularis density, increased oxidative stress, cell apoptosis, and decreased antioxidant levels. High glucose exposure increased apoptosis and ROS content in pericytes, while mitochondrial membrane potential decreased, with AIF and cytochrome C (CytC) released from mitochondria to the cytoplasm. Adding oxidative scavengers reduced AIF and CytC release, decreasing pericyte apoptosis.
UNASSIGNED: Hyperglycemia may induce mitochondrial apoptosis of cochlear stria vascularis pericytes through oxidative stress.
摘要：
■糖尿病与听力损失密切相关，然而，确切的机制仍不清楚。耳蜗血管纹和周细胞（PC）对听力至关重要。这项研究调查了高葡萄糖是否通过氧化应激引起的ROS水平升高而诱导耳蜗血管纹和周细胞凋亡。影响听力损失。
■我们在C57BL/6J小鼠中建立了II型糖尿病模型，并使用听觉脑干反应（ABR），伊文思蓝染色,HE染色,免疫组织化学，和免疫荧光来观察听力的变化，血迷宫屏障（BLB）通透性，血管纹形态，和凋亡蛋白表达。原代培养的血管纹周细胞接受高糖治疗，和凋亡水平使用流式细胞术评估，膜联蛋白V-FITC,Hoechst33342染色,蛋白质印迹,Mitosox,和JC-1探测器。
■糖尿病小鼠显示听力阈值下降，血管纹密度降低，氧化应激增加，细胞凋亡，和降低抗氧化剂水平。高糖暴露会增加周细胞的凋亡和ROS含量，而线粒体膜电位下降，AIF和细胞色素C（CytC）从线粒体释放到细胞质。添加氧化清除剂减少AIF和CytC释放，减少周细胞凋亡。
■高血糖可能通过氧化应激诱导耳蜗血管周细胞线粒体凋亡。
■我们在C57BL/6J小鼠中建立了II型糖尿病模型，并使用听觉脑干反应（ABR），伊文思蓝染色,HE染色,免疫组织化学，和免疫荧光来观察听力的变化，血迷宫屏障（BLB）通透性，血管纹形态，和凋亡蛋白表达。原代培养的血管纹周细胞接受高糖治疗，和凋亡水平使用流式细胞术评估，膜联蛋白V-FITC,Hoechst33342染色,蛋白质印迹,Mitosox,和JC-1探测器。
■糖尿病小鼠显示听力阈值下降，血管纹密度降低，氧化应激增加，细胞凋亡，和降低抗氧化剂水平。高糖暴露会增加周细胞的凋亡和ROS含量，而线粒体膜电位下降，AIF和细胞色素C（CytC）从线粒体释放到细胞质。添加氧化清除剂减少AIF和CytC释放，减少周细胞凋亡。
■高血糖可能通过氧化应激诱导耳蜗血管周细胞线粒体凋亡。
