Modified Wuzi Yanzong Prescription Inhibited Tau Protein Hyperphosphorylation induced by A-in PC12 Cells

ZENG Ke-wu; WANG Xue-mei; FU Hong; LIU Geng-xin

doi:CNKI:11-3495/R.20110314.0942.009

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Modified Wuzi Yanzong Prescription Inhibited Tau Protein Hyperphosphorylation induced by A-in PC12 Cells

更新时间：2024-01-04

- Modified Wuzi Yanzong Prescription Inhibited Tau Protein Hyperphosphorylation induced by A-in PC12 Cells
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 17, Issue 9, Pages: 159-163(2011)
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- DOI：CNKI:11-3495/R.20110314.0942.009
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- Published：2011
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ZENG Ke-wu, WANG Xue-mei, FU Hong, et al. Modified Wuzi Yanzong Prescription Inhibited Tau Protein Hyperphosphorylation induced by A-in PC12 Cells[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(9): 159-163.
DOI：

ZENG Ke-wu, WANG Xue-mei, FU Hong, et al. Modified Wuzi Yanzong Prescription Inhibited Tau Protein Hyperphosphorylation induced by A-in PC12 Cells[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(9): 159-163. DOI： CNKI:11-3495/R.20110314.0942.009.

摘要

目的: 研究加味五子衍宗方对β-淀粉样蛋白(β-amyloid protein

Aβ25-35)所致的大鼠肾上腺嗜铬细胞瘤细胞株(PC12)中的微管相关蛋白(tau蛋白)高度磷酸化的抑制作用和潜在机制。方法: 将PC12细胞分为正常对照组、模型组、给药组

使用Aβ25-35(30 μmol ·L-1)诱导PC12细胞的tau蛋白高度磷酸化

并同时加入加味五子衍宗方提取物(50~400 mg ·L-1)作用细胞24 h

然后考察加味五子衍宗方对PC12细胞tau蛋白高度磷酸化的抑制作用。结果: 加味五子衍宗方单独作用细胞后

无明显毒性作用。但是加味五子衍宗方可以显著的抑制Aβ25-35所诱导的神经毒性

细胞存活率由损伤组的70%±4.9%提高到治疗组的98%±6.5%(P<0.01);且凋亡相关蛋白Caspase-3和PARP的表达也受到了显著性的抑制

分别从损伤组的378.15%±34.65%和985.12%±45.32%降低到治疗组的127.65%±12.65%和543.61%±39.07%(P<0.01)。此外

PC12细胞中tau蛋白的高度磷酸化也出现了显著下调

Ser396位点的磷酸化水平从损伤组的130.01%±5.83%降低到治疗组的113.75%±6.34%(P<0.01)

Ser404位点的磷酸化水平从损伤组的150.17%±10.28%降低到治疗组的105.37%±4.57%(P<0.01)

其机制可能是通过抑制糖原合酶激酶(glycogen synthase kinase 3β

GSK-3β)在Ser9位点的磷酸化以及促分裂素原活化蛋白激酶(mitogen-activated protein kinases

MAPK)的磷酸化来实现的。结论: 加味五子衍宗方可以有效的抑制Aβ25-35所致的PC12细胞中tau蛋白的高度磷酸化

具有潜在的治疗阿尔茨海默病的作用。

Abstract

Objective: To investigate the neuroprotective effect of modified Wuzi Yanzong prescription (MWP)on β-amyloid protein (Aβ25-35)-induced tau protein hyperphosphorylation in PC12 cells and the potential mechanism. Method: Control

Aβ25-35 model and sample treatment groups were set in our study. Aβ25-35(30 μmol ·L-1)was used to induce tau protein hyperphosphorylation in PC12 cells

and MWP(50-400 mg ·L-1)was also simultaneously added. Then

the neuroprotective effects of MWP were investigated. Result: MWP alone did not show any cytotoxicity in PC12 cells. MWP significantly protected PC12 cells from Aβ25-35-induced neurotoxicity

cell viability increased from (70±4.9)% to (98±6.5)%(P<0.01)

and apoptosis-related protein (Caspase-3 and PARP)expressions were also effectively inhibited

Caspase-3 and PARP were down-regulated from (378.15±34.65)% and (985.12±45.32)% to (127.65±12.65)% and (543.61±39.07)%(P<0.01). In addition

tau protein hyperphosphorylation in PC12 cells was significantly down-regulated

p-tau (in Ser396 site) expression decreased from (130.01±5.83)% to (113.75±6.34)%(P<0.01)

and p-tau (in Ser404 site) expression decreased from (150.17±10.28)% to (105.37±4.57)%(P<0.01). The inhibitory effects of MWP on the phosphorylation of glycogen synthase kinase 3β(GSK-3β)at Ser9 site and mitogen-activated protein kinases (MAPK) may explain the potential mechanism. Conclusion: MWP could inhibit Aβ25-35-induced tau protein hyperphosphorylation on PC12 cells

showing a neuroprotective effect in Alzheimer’s disease.

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