Tatsumi Yasuko, Kanamori Akiyasu, Nagai-Kusuhara Azusa, Nakanishi Yoriko, Agarwal Neeraj, Negi Akira, Nakamura Makoto
Department of Surgery, Division of Ophthalmology, Kobe University Graduate School of Medicine, Kobe, Japan.
Curr Eye Res. 2008 Aug;33(8):683-92. doi: 10.1080/02713680802323157.
To investigate if nipradilol has an anti-apoptotic effect in serum-deprived RGC-5 cells and in the streptozotocin-induced diabetic rat retina.
Apoptosis was quantified by activated caspase-3 immunohistochemistry or terminal dUTP nick end-labeling assay.
Nipradilol dose-dependently suppressed apoptosis in a protein kinase A- and G-dependent manner and counteracted glutamate-induced calcium entry in the RGC-5 cells and reduced apoptotic cells in the retinal ganglion cell layer of 4- and 12-week diabetic retinas compared to controls when instilled for 5 days. Removal of the nitric oxide moiety from nipradilol blocked these effects.
Nipradilol protects RGCs from apoptosis induced by serum-deprivation in vitro and by diabetes in vivo. The NO-related signaling pathway mediates the anti-apoptotic ability of nipradilol.
研究尼普地洛对血清剥夺的RGC - 5细胞以及链脲佐菌素诱导的糖尿病大鼠视网膜是否具有抗凋亡作用。
通过活化的半胱天冬酶 - 3免疫组织化学或末端脱氧核苷酸转移酶介导的缺口末端标记法对细胞凋亡进行定量分析。
尼普地洛以蛋白激酶A和G依赖性方式剂量依赖性地抑制细胞凋亡，抵消谷氨酸诱导的RGC - 5细胞钙内流，并在滴注5天后，与对照组相比，减少4周和12周糖尿病视网膜神经节细胞层中的凋亡细胞。从尼普地洛中去除一氧化氮部分会阻断这些作用。
尼普地洛在体外可保护RGCs免受血清剥夺诱导的凋亡，在体内可保护其免受糖尿病诱导的凋亡。与一氧化氮相关的信号通路介导了尼普地洛的抗凋亡能力。
