Effect of  Saponins Protect PC12 Cell Against Hydrogen Peroxide Induced Damage

XIA Xing; ZHONG Zhen-guo; FENG Dan-xia

您当前的位置：

首页 >

文章列表页 >

Effect of Saponins Protect PC12 Cell Against Hydrogen Peroxide Induced Damage

更新时间：2024-01-04

- Effect of Saponins Protect PC12 Cell Against Hydrogen Peroxide Induced Damage
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 19, Issue 4, Pages: 216-219(2013)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：
  CLC：
- Published：2013
- 稿件说明：
移动端阅览
XIA Xing, ZHONG Zhen-guo, FENG Dan-xia. Effect of Saponins Protect PC12 Cell Against Hydrogen Peroxide Induced Damage[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(4): 216-219.
DOI：

XIA Xing, ZHONG Zhen-guo, FENG Dan-xia. Effect of Saponins Protect PC12 Cell Against Hydrogen Peroxide Induced Damage[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(4): 216-219. DOI：

摘要

目的: 考察三七总皂苷在PC12细胞中对过氧化氢引起损伤的细胞保护作用。方法: 采用MTT法考察0.01~100 mg·L-1三七总皂苷对正常PC12细胞活力的影响

并在H2O2刺激的PC12细胞中考察0.1~10 mg·L-1的三七总皂苷对细胞活力的影响

通过对细胞活力的考察选择三七总皂苷合适的实验剂量

测定三七总皂苷0.1

1 mg·L-1对H2O2刺激的PC12细胞中活性氧水平、过氧化氢酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力的影响以及对丙二醛(MDA)含量的影响。结果: 三七总皂苷在0.1~10 mg·L-1浓度能提高正常PC12细胞活力

并能显著提高H2O2刺激的PC12细胞活力(P<0.01)。0.1

1 mg·L-12个剂量的三七总皂苷均能显著减少H2O2刺激的PC12细胞中活性氧水平

提高SOD活力(P<0.001)和GSH-Px活力(P<0.001)

并减少MDA生成(P<0.001)。结论: 三七总皂苷能通过增强细胞内抗氧化酶活力

保护PC12细胞对抗氧化损伤。

Abstract

Objective: To investigate the protective effect of Panax notoginseng saponins (PNS) on hydrogen peroxide (H2O2) induced oxidative damage in PC12 cell. Method: MTT method was employed to determine the viability in PNS (0.01-100 mg·L-1) treated PC12 cell and PNS (0.1-10 mg·L-1) plus H2O2 treated PC12 cell. Thereafter

intracellular reactive oxygen species amounts

activity of SOD

GSH-Px

as well as MDA concentration were determined at optimal dosage of PNS selected based on MTT experiment. Result: PC12 cell viability was increased by PNS at 0.1-10 mg·L-1

and the viability of H2O2 treated PC12 cell was increased by PNS at 0.1-10 mg·L-1. Furthermore

PNS at 0.1-1.0 mg·L-1 significantly decreased intracellular reactive oxygen species levels

as well as enhanced SOD activity (P<0.001) and GSH-Px activity (P<0.001). But MDA concentration was decreased significantly (P<0.05). Conclusion: PNS can protect PC12 cell against H2O2 induced damage via enhancement of intracellular antioxidant enzyme activity.

关键词

Keywords

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Zhenwutang Ameliorates Diabetic Kidney Disease in Mice with Spleen-kidney Yang Deficiency via Nrf2/HO-1/GPX4 Signaling Pathway

Correlation Analysis Between Anti-cerebral Ischemia Oxidative Damage and Contents of Active Components in Characteristic Processed Products with Porcine Cardiac Blood and Other Processed Products of Salviae Miltiorrhizae Radix et Rhizoma from Menghe Medical School

Regulatory Mechanism of Berberine in Inhibiting Apoptosis and Autophagy in Ovarian Granulosa Cells Based on SIRT1/FoxO1 Pathway

Naoxin'an Capsule Alleviates Mitochondrial and Oxidative Damage in Chronic Cerebral Ischemia-induced VCI in Rats via Activating CREB/PGC-1α Pathway

Effect of Buyang Huanwutang on Keap1/Nrf2/HO-1 Antioxidant Signaling Pathway in Rats with Idiopathic Pulmonary Fibrosis

Related Author

ZHAO Zhe

CHEN Guangshun

BAI Min

JIN Yuqiu

TIAN Mengyuan

SONG Bing

LIU Zhenhua

ZHANG Yanying

Related Institution

Gansu Laboratory Animal Industry Technology Center

Gansu University of Chinese Medicine

Changzhou Key Laboratory of Human Use Experience Research&Transformation of Menghe Medical School，Changzhou Hospital of Traditional Chinese Medicine， Nanjing University of Chinese Medicine

School of Life Sciences，Beijing University of Chinese Medicine

School of Traditional Chinese Medicine， Beijing University of Chinese Medicine

AI问答

Postal code：100700
Tel：010-84076882 Email：syfjx_2010@188.com
Technical support is provided by Beijing Founder electronics co., LTD 京ICP备11006657号-10 京公网安备11010802024621
It is recommended to read the content of this site in Chrome&IE9+. Please switch to extreme mode in browser 360.
Cookies We use cookies to help provide and enhance our service and tailor content. By continuing, you agree to the use of cookies.

⁰