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纸质出版日期:2018
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温萍, 陈盛铎, 郑兵, 等. 金蝉花多糖对-GlaN致小鼠急性肝损伤的保护作用及机制[J]. 中国实验方剂学杂志, 2018,24(6):108-113.
WEN Ping, CHEN Sheng-duo, ZHENG Bing, et al. Protective Effect and Mechanism of Polysaccharides from on Acute Liver Injury Induced by -GlaN in Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(6): 108-113.
温萍, 陈盛铎, 郑兵, 等. 金蝉花多糖对-GlaN致小鼠急性肝损伤的保护作用及机制[J]. 中国实验方剂学杂志, 2018,24(6):108-113. DOI: 10.13422/j.cnki.syfjx.20180630.
WEN Ping, CHEN Sheng-duo, ZHENG Bing, et al. Protective Effect and Mechanism of Polysaccharides from on Acute Liver Injury Induced by -GlaN in Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(6): 108-113. DOI: 10.13422/j.cnki.syfjx.20180630.
目的:观察金蝉花多糖对D-半乳糖胺(D-galactosamine,D-GlaN)致小鼠急性肝损伤的保护作用,并初步探讨其作用机制。方法: 75只雄性昆明小鼠根据数字表法随机分为5组,每组15只,正常组,腹腔注射生理盐水;模型组,腹腔注射D-GlaN;金蝉花多糖低、中、高剂量组,腹腔注射D-GlaN的同时予以金蝉花多糖溶液(0.5,1.0,2.0 g ·kg-1)灌胃治疗。治疗12 d后检测各组肝组织病理评分、肝匀浆指标[超氧化物歧化物(superoxide dismutase,SOD),丙二醛(malondialdehyde,MDA),谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px),一氧化氮(nitric oxide,NO)],血清学指标[天门冬氨酸氨基转移酶(aspartate transaminase,AST),丙氨酸氨基转移酶(alanine transaminase,ALT),碱性磷酸酶(alkaline phosphatase,ALP),胆碱酯酶(cholinesterase,CHE)],采用免疫组化法检测各组肝组织核转录因子-κB (nuclear transcription factor-κB,NF-κB),肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)表达水平。结果:模型组肝组织病理评分,MDA,NO,AST,ALT,ALP,NF-κB,TNF-α水平均明显高于正常组(P<0.05),而SOD,GSH-Px,CHE水平明显低于正常组(P<0.05);金蝉花多糖低、中、高剂量组肝组织病理评分均明显低于模型组(P<0.05),且随治疗剂量升高,肝组织病理评分呈明显降低趋势(P<0.05);金蝉花多糖低、中、高剂量组MDA,NO,AST,ALT,ALP,NF-κB,TNF-α水平均明显低于模型组(P<0.05),而SOD,GSH-Px,CHE水平均明显高于模型组(P<0.05),且随治疗剂量升高,MDA,NO,AST,ALT,ALP,NF-κB,TNF-α水平明显降低(P<0.05),而SOD,GSH-Px,CHE水平明显升高(P<0.05)。结论:金蝉花多糖对D-GlaN致小鼠急性肝损伤具有明显的保护作用,且呈剂量依赖性,其作用机制可能为抑制NF-κB炎性反应信号通路有关。
Objective: To observe the protective effect of polysaccharides from Cordyceps cicadae on acute liver injury induced by D-galactosamine (D-GlaN) in mice
and to explore its mechanism.Method: Seventy-five male Kunming mice were randomly divided into 5 groups (n=15 for each group). The miceinnormal group were injected with saline solution intraperitoneally while the mice in model group were intraperitoneally injected with D-GlaN. The mice in polysaccharides from C. cicadae low dose
middle dose and high dose groups were intraperitoneally injected with D-GlaN and lavage treatment with polysaccharides from C. cicadae solution (0.5
1.0
2.0 g · kg-1 respectively). After 12 days of treatment
the mouse liver homogenate indexes[superoxide dismutase (SOD)
malondialdehyde(MDA)
glutathione peroxidase(GSH-Px)
nitric oxide(NO)]
and serum markers[aspartate transaminase(AST)
alanine transaminase(ALT)
alkaline phosphatase(ALP)
cholinesterase(CHE)]were detected together withthe liver tissue pathological scores in each groups. The expression levels of nuclear transcription factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α) were detected in the liver tissues by immunohistochemistry.Result: The liver histopathological scores
MDA
NO
AST
ALT
ALP
NF-κB
and TNF-α in model group were significantly higher than those in normal group (P<0.05)
while the levels of SOD
GSH-Px and CHE were significantly lower than those in normal group(P<0.05). The liver histopathological scores in the polysaccharides from C. cicadae low
middle and high dose groups were significantly lower than those in model group (P<0.05)
moreover
the liver histopathological scores tended to decrease with the increase of therapeutic dose (P<0.05); the levels of MDA
NO
AST
ALT
ALP
NF-κB
and TNF-α in the low
middle and high dose groups were significantly lower than those in model group (P<0.05)
while the levels of SOD
GSH-Px and CHE were significantly higher than those in the model group (P<0.05)
and as the therapeutic dose increased
the levels of MDA
NO
AST
ALT
ALP
NF-κB and TNF-α were significantly decreased (P<0.05)
while SOD
GSH-Px
CHE levels were significantly increased (P<0.05).Conclusion: Polysaccharides from C. cicadae may have protective effect on D-GlaN-induced acute liver injury in a dose-dependent manner
and its mechanismmay be related to the inhibition of NF-κB inflammatory signaling pathway.
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