XQ-1H attenuates ischemic injury in PC12 cells via Wnt/β-catenin signaling though inhibition of apoptosis and promotion of proliferation.,Cell Biology International

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XQ-1H attenuates ischemic injury in PC12 cells via Wnt/β-catenin signaling though inhibition of apoptosis and promotion of proliferation.
Cell Biology International ( IF 3.3 ) Pub Date : 2020-08-06 , DOI: 10.1002/cbin.11438
Dan Xu ₁ , Fengyang Li ₁ , Kai Hou ₂ , Xue Gou ₁ , Weirong Fang ₁ , Yunman Li ₁

Affiliation

10‐O‐(N,N‐dimethylaminoethyl)‐ginkgolide B methanesulfonate (XQ‐1H) is a new derivative of ginkgolide B and has previously been proven to exert neuroprotective effects on ischemic injury. However, it is not clear whether XQ‐1H affects the cell survival and proliferation in oxygen–glucose deprivation/reoxygenation (OGD/R) damaged PC12 cells. Our results showed that OGD/R improved cell viability after 24 hr of posttreatment with XQ‐1H (10 or 5 μM), inhibiting cell injury and apoptosis by upregulating the expression of brain‐derived neurotrophic factor, nerve growth factor, and antiapoptotic B‐cell lymphoma‐extra large, while reducing proapoptotic cleaved caspase‐3 protein. By introducing the Wnt/β‐catenin signaling inhibitor XAV‐939 and 5‐bromo‐2′‐deoxyuridine staining, it was proved that XQ‐1H promoted the proliferation of PC12 cells in a Wnt‐signal‐dependent manner via inhibiting the activation of glycogen synthase kinase‐3β after phosphatidylinositol 3‐kinase/protein kinase B signal activation, thereby activating Wnt1, β‐catenin, and the expression of downstream neurogenic differentiation 1 and cyclin D1, which was comparable to Wnt/β‐catenin signaling agonist 4,6‐disubstituted pyrrolopyrimidine. We conclude that XQ‐1H, after OGD/R damage to PC12 cells, may limit cell apoptosis in a Wnt/β‐catenin signal‐dependent manner, promoting cell proliferation and survival.

中文翻译：

XQ-1H通过抑制细胞凋亡和促进增殖，通过Wnt /β-catenin信号传导减轻PC12细胞的缺血性损伤。

10‐O‐（N，N-二甲基氨基乙基）-银杏内酯B甲磺酸盐（XQ-1H）是银杏内酯B的新衍生物，先前已被证明对缺血性损伤具有神经保护作用。但是，目前尚不清楚XQ-1H是否会在受损的PC12细胞中发生氧-葡萄糖剥夺/复氧（OGD / R）的细胞存活和增殖。我们的结果表明，OGD / R可在XQ-1H（10或5μM）后处理24小时后改善细胞活力，通过上调脑源性神经营养因子，神经生长因子和抗凋亡B-的表达来抑制细胞损伤和凋亡。细胞淋巴瘤过大，同时减少凋亡前体裂解的caspase-3蛋白。通过引入Wnt /β-catenin信号抑制剂XAV-939和5-bromo-2'-脱氧尿苷染色，证明XQ-1H通过抑制磷脂酰肌醇3激酶/蛋白激酶B信号激活后糖原合酶激酶3β的激活，从而以Wnt信号依赖性的方式促进PC12细胞的增殖，从而激活Wnt1，β-catenin ，以及下游神经源性分化1和细胞周期蛋白D1的表达，与Wnt /β-catenin信号激动剂4,6-二取代的吡咯并嘧啶具有可比性。我们得出的结论是，OGD / R损伤PC12细胞后，XQ-1H可能以Wnt /β-catenin信号依赖性方式限制细胞凋亡，从而促进细胞增殖和存活。下游神经原性分化1和细胞周期蛋白D1的表达，可与Wnt /β-catenin信号激动剂4,6-二取代吡咯并嘧啶媲美。我们得出的结论是，OGD / R损伤PC12细胞后，XQ-1H可能以Wnt /β-catenin信号依赖性方式限制细胞凋亡，从而促进细胞增殖和存活。下游神经原性分化1和细胞周期蛋白D1的表达，可与Wnt /β-catenin信号激动剂4,6-二取代吡咯并嘧啶媲美。我们得出的结论是，OGD / R损伤PC12细胞后，XQ-1H可能以Wnt /β-catenin信号依赖性方式限制细胞凋亡，从而促进细胞增殖和存活。

更新日期：2020-10-13

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