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纸质出版日期:2018
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陈春, 陈毅飞, 曹后康, 等. 酢浆草对四氯化碳致急性肝损伤大鼠的保护作用及机制[J]. 中国实验方剂学杂志, 2018,24(16):141-145.
CHEN Chun, CHEN Yi-fei, CAO Hou-kang, et al. Protective Effect and Mechanism of Oxalidis Corniculatase Herba on Acute Hepatic Injury Induced by Carbon Tetrachloride in Rats[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(16): 141-145.
陈春, 陈毅飞, 曹后康, 等. 酢浆草对四氯化碳致急性肝损伤大鼠的保护作用及机制[J]. 中国实验方剂学杂志, 2018,24(16):141-145. DOI: 10.13422/j.cnki.syfjx.20181627.
CHEN Chun, CHEN Yi-fei, CAO Hou-kang, et al. Protective Effect and Mechanism of Oxalidis Corniculatase Herba on Acute Hepatic Injury Induced by Carbon Tetrachloride in Rats[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(16): 141-145. DOI: 10.13422/j.cnki.syfjx.20181627.
目的:拟从Toll样受体-2(TLR-2)/核转录因子-κB(NF-κB)信号通路,探讨酢浆草对四氯化碳(CCl4)致急性肝损伤大鼠的保护作用及其机制。方法: 48只雌性大鼠随机分为正常组,模型组,水飞蓟素(0.12 g·kg-1)组和酢浆草高、中、低剂量(16,8,4 g·kg-1)组,每组8只。除正常组及模型组给予等体积蒸馏水外,各给药组按5 mL·kg-1灌胃给药,每天按时灌胃2次,共10 d。末次给药2 h后,除正常组以外,其余各组均腹腔注射12% CCl4橄榄油溶液(5 mL·kg-1)建立大鼠肝损伤模型。16 h后,眼球取血,取肝组织制备肝组织切片。生化法检测血清中天门冬氨酸氨基转移酶(AST),丙氨酸氨基转移酶(ALT),总超氧化物歧化酶(T-SOD),谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量。酶联免疫吸附法(ELISA)检测血清中肿瘤坏死因子-α(TNF-α),白细胞介素-1β(IL-1β)和IL-6含量,蛋白免疫印迹法(Western blot)检测肝组织中TLR-2与NF-κB蛋白的表达;光镜下观察肝组织结构。结果:与正常组比较,模型组血清中ALT,AST活性和MDA,IL-1β,IL-6,TNF-α水平显著升高(P<0.01),血清中GSH-Px,T-SOD活性显著降低(P<0.01);肝组织中TLR-2,NF-κB蛋白表达显著增强(P<0.01),模型组大鼠肝损伤较为明显。与模型组比较,酢浆草各剂量组血清中ALT,AST活性和MDA含量明显降低(P<0.05,P<0.01),血清中GSH-Px,T-SOD活性明显升高(P<0.05,P<0.01),IL-1β,IL-6及TNF-α水平,TLR-2,NF-κB蛋白表达明显下降(P<0.05,P<0.01);肝组织切片显示酢浆草对CCl4致急性肝损伤大鼠有改善作用。结论:酢浆草对CCl4致急性肝损伤大鼠具有保护作用,其机制可能干预TLR-2/NF-κB信号通路和抑制氧化应激的作用有关。
Objective: To investigate the protective effect and related mechanism of Oxalidis Coriniculatose Herba on acute hepatic injury induced by carbon tetra-chloride in rats based on Toll-like-receptor-2 (TLR-2)/nuclear factor-kappa B (NF-κB) signaling pathway. Method: A total of 48 female rats were randomly divided into normal group
model group
silymarin (0.12 g·kg-1) group
and high
middle and low-dose Oxalidis Corniculatase Herba(16
8
4 g·kg-1) groups
with 8 in each group. Except for the normal group and model group
all of the remaining rats were given drugs by gavage for 10 days
twice a day. Two hours later
except for the normal group
all of the remaining rats were injected with 12% carbon tetra-chloride olive oil solution (5 mL·kg-1) via abdominal cavity to establish the acute liver injury model. After 16 hours
the blood was taken from the retrobulbar arteries
and the liver tissues were collected to make htoxylin eosin(HE) pathological sections. The activity of alanine aminotransferase (ALT)
aspartate aminotransferase (AST)
total-superoxide dismutase (T-SOD)
glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in serum of rats were detected by biochemical method. The level of tumor necrosis factor alpha (TNF-α)
interleukin-1 β(IL-1β) and interleukin-6 (IL-6) in serum were assayed by enzyme linked immuno sorbent assay (ELISA); and protein expressions of TLR-2 and NF-κB in liver tissue of rats were tested by Western blot. HE pathological sections of liver tissues of rats were observed under microscope. Result: Compared with the normal group
the serum activity of ALT
AST and the content of MDA significantly increased
whereas T-SOD and GSH-Px activity decreased (P<0.01)
and the levels of IL-1β
TNF-α
IL-6 in serum and the hepatic expressions of TLR-2
NF-κB increased in the model group (P<0.01). After intervention with Oxalidis Corniculatase Herba
the activities of ALT
AST and the levels of MDA
IL-1β
IL-6
TNF-α in serum were obviously reduced (P<0.05
P<0.01)
while the activities of GSH-Px and SOD in serum were improved (P<0.05
P<0.01)
and the expressions of TLR-2 and NF-κB in liver tissue were inhibited (P<0.05
P<0.01). The pathological sections also showed that the liver injury degree in rats was significantly alleviated. Conclusion: Oxalidis Corniculatase Herba can ease the acute liver injury in rats induced by carbon tetra-chloride olive oil solution
the mechanism may be related with the intervention of TLR-2/NF-κB signaling pathway and the inhibition of oxidative stress and inflammatory responses.
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