Influences of Mongolian Medicine Dedu Honghua Qiwei Powder on Liver Mitochondrial Energy Metabolism in Rat with Chronic Liver Injury

HAN Zhi-qiang; BA Tu-de-li-gen; GAO Yu-feng; NA Ri-su; E Er-deng-bi-li-ge

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Influences of Mongolian Medicine Dedu Honghua Qiwei Powder on Liver Mitochondrial Energy Metabolism in Rat with Chronic Liver Injury

更新时间：2024-09-23

- Influences of Mongolian Medicine Dedu Honghua Qiwei Powder on Liver Mitochondrial Energy Metabolism in Rat with Chronic Liver Injury
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 19, Issue 5, Pages: 270-273(2013)
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- Published：2013
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HAN Zhi-qiang, BA Tu-de-li-gen, GAO Yu-feng, et al. Influences of Mongolian Medicine Dedu Honghua Qiwei Powder on Liver Mitochondrial Energy Metabolism in Rat with Chronic Liver Injury[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(5): 270-273.
DOI：

HAN Zhi-qiang, BA Tu-de-li-gen, GAO Yu-feng, et al. Influences of Mongolian Medicine Dedu Honghua Qiwei Powder on Liver Mitochondrial Energy Metabolism in Rat with Chronic Liver Injury[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(5): 270-273. DOI：

摘要

目的: 观察德都红花-7味散对四氯化碳(CCl4)所致慢性肝损伤线粒体能量代谢的影响。方法: 将Wistar雄性大鼠随机分为空白对照组、模型组、秋水仙碱阳性对照组、德都红花-7味散低、高剂量组

每组8只。除空白对照组

其他组均腹腔注射30% CCl4橄榄油溶液2.0 mL·kg-1

1周2次

连续7周。空白对照组和模型组灌胃蒸馏水

秋水仙碱组以0.4 mg·kg-1

德都红花-7味散低剂、高剂量组以(0.62

1.04 g·kg-1)

灌胃给药

连续7周。末次给药后取肝脏

肝左叶制备肝线粒体

肝组织匀浆

检测肝线粒体钠钾三磷酸腺苷酶(Na+-K+-ATP酶)活性和肝组织匀浆超氧化物歧化酶(SOD)

丙二醛(MDA)含量;高效液相色谱(HPLC)方法检测肝线粒体三磷酸腺苷(ATP)

二磷酸腺苷(ADP)

一磷酸腺苷(AMP)含量

计算能荷(ED)。结果 : 与空白对照组比较模型组SOD

Na+-K+-ATP酶活性明显下降

MDA含量升高

秋水仙碱组Na+-K+-ATP酶活性明显下降(P＜0.05);与模型组比较秋水仙碱组、德都红花-7味散低、高剂量组肝组织SOD活性明显升高

MDA含量明显降低

德都红花-7味散低、高剂量组肝线粒体Na+-K+-ATP酶活性明显升高(P＜0.05)。与空白组比较

模型组ATP

ADP含量和ED明显降低(P＜0.05)。与模型组比较德都红花-7味散高、低剂量组和秋水仙碱组ATP

ADP含量和ED明显升高(P＜0.05)。结论 :德都红花-7味散可能通过抗脂质过氧化

保护肝线粒体能量代谢

发挥保护CCl4所致慢性肝损伤。

Abstract

Objective:To observe the influence of Dedu Honghua Qiwei powder (DHQP) on liver mitochondrial energy metabolism in rats with chronic liver injury induced by Carbon tetrachloride(CCl4). Method: Male Wistar rats were randomly divided into blank control group

model group

colchicine positive control group

DHQP low and high dose groups based on body weight

8 rats in each group. Except the blank control group

other groups were injected intraperitoneally 30% of CCl4 olive oil solution 20 mL·kg-1

twice a week

continued for 7 weeks. Blank control group and model group were given distilled water orally; colchicine group was given 0.4 mg·kg-1

DHQP low-dose group and high-dose group were given 0.62

1.04 g·kg-1 respectively

20 mL·kg-1

bid

continued for 7 weeks. Forty-eight hours after last administration

the rats were fasted 12 hours

and then anesthetized by 10% of chloral hydrate 0.3 mL·kg-1

blood was collected. Liver was taken out immediately

and the left lobe of liver was used to make liver homogenates

then sodium potassium adenosine triphosphatase(Na+-K+-ATPase)activity of liver mitochondrial and superoxide dismutase (SOD)

malondialdehyde (MDA) content of liver tissue were measured. High performance liquid chromatography (HPLC) was used to measure the liver mitochondrial adenosine triphosphate (ATP)

adenosine diphosphate (ADP)

adenosine monophosphate (AMP) and the energy charge was calculated. Result: Compared with blank control group

model group's SOD

Na+-K+-ATPase activity were decreased significantly

MDA contents was increased

colchicine group's Na+-K+-ATPase activity was decreased significantly (P<0.05). Compared with model group

the colchicine group

DHQP high

low dose group's liver mitochondrial Na+-K+-ATPase activity was significantly increased (P<0.05). Compared with blank control group

modeling group's ATP

ADP contents and ED decreased significantly(P<0.05). Compared with model group

DHQP high

low dose group and colchicine group's ATP

ADP contents and ED were significantly increased (P<0.05). Conclusion: DHQP may act an anti-lipid peroxidation role to protect the liver mitochondrial energy metabolism

and act a role as protecting the chronic liver injury.

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Related Author

HAN Zhi-qiang

BA Tu-de-li-gen

GAO Yu-feng

NA Ri-su

E Er-deng-bi-li-ge

ZHAO Jinghan

ZHU Zhengwang

WANG Linlin

Related Institution

Institute of Clinical Pharmacology of Traditional Mongolian Medicine,Affiliated Hospital of Inner Mongolia University for the Nationalities

The First Clinical Medical College of Henan University of Chinese Medicine

School of Pharmacy， Henan University of Chinese Medicine

Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-yao

Institute of Chinese Materia Medica，China Academy of Chinese Medical Sciences

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