首都医科大学学报
首都醫科大學學報
수도의과대학학보
JOURNAL OF CAPITAL UNIVERSITY OF MEDICAL SCIENCES
2014年
6期
813-817
,共5页
贾丽超%周明学%张蕾%刘卫红
賈麗超%週明學%張蕾%劉衛紅
가려초%주명학%장뢰%류위홍
当归芍药散%代谢性炎性反应%脂代谢紊乱%动脉粥样硬化
噹歸芍藥散%代謝性炎性反應%脂代謝紊亂%動脈粥樣硬化
당귀작약산%대사성염성반응%지대사문란%동맥죽양경화
Dangguishaoyaosan%metaflammation%dyslipidemia%atherosclerosis
目的:研究当归芍药散对代谢性炎性反应小鼠血脂和血清炎性反应因子白细胞介素-6(interleukin-6,IL-6)、单核细胞趋化蛋白-1(monocyte chemotactic protein 1,MCP-1)以及核因子κB (nuclear factor kappa B,NF-κB)和活化的过氧化物酶体增生物激活受体γ(peroxisome proliferator-activated receptor gamma,PPARγ)mRNA 表达的影响。方法60只雄性 C57小鼠,采用数字表法将动物随机分为正常组、模型组、立普妥组、当归芍药散组(n =15)。采用高脂饮食联合脂多糖注射造成小鼠代谢性炎性反应模型。造模5周后,开始灌胃给药,每天2次,当归芍药散2.2 g/ kg,立普妥0.003 g/ kg。正常对照组和模型组灌服等体积蒸馏水。连续灌胃5周。处死后采血和取肝脏,检测各组小鼠血清胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)和低密度脂蛋白胆固醇(low density lipoprotein,LDL-C)浓度,并采用流式细胞术检测血清炎性反应因子 IL-6和 MCP-1浓度。反转录聚合酶链式反应(reverse transcription polymerase chain reaction,RT-PCR)法测定肝脏 NF-κB 和 PPARγmRNA 的表达。结果与模型组相比,当归芍药散组小鼠血清 TC 和 LDL-C 水平明显降低(P<0.01),肝脏组织中 NF-κB mRNA 的表达降低,差异有统计学意义(P<0.05),PPARγmRNA 的表达提高,差异有统计学意义(P<0.05)。结论当归芍药散可降低代谢性炎性反应小鼠血脂和血清炎性反应因子 IL-6和 MCP-1浓度,并可通过调控核转录因子 NF-κB 和 PPARγ受体,抑制小鼠体内代谢性炎性反应,从而可能对早期动脉粥样硬化起到干预作用。
目的:研究噹歸芍藥散對代謝性炎性反應小鼠血脂和血清炎性反應因子白細胞介素-6(interleukin-6,IL-6)、單覈細胞趨化蛋白-1(monocyte chemotactic protein 1,MCP-1)以及覈因子κB (nuclear factor kappa B,NF-κB)和活化的過氧化物酶體增生物激活受體γ(peroxisome proliferator-activated receptor gamma,PPARγ)mRNA 錶達的影響。方法60隻雄性 C57小鼠,採用數字錶法將動物隨機分為正常組、模型組、立普妥組、噹歸芍藥散組(n =15)。採用高脂飲食聯閤脂多糖註射造成小鼠代謝性炎性反應模型。造模5週後,開始灌胃給藥,每天2次,噹歸芍藥散2.2 g/ kg,立普妥0.003 g/ kg。正常對照組和模型組灌服等體積蒸餾水。連續灌胃5週。處死後採血和取肝髒,檢測各組小鼠血清膽固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)和低密度脂蛋白膽固醇(low density lipoprotein,LDL-C)濃度,併採用流式細胞術檢測血清炎性反應因子 IL-6和 MCP-1濃度。反轉錄聚閤酶鏈式反應(reverse transcription polymerase chain reaction,RT-PCR)法測定肝髒 NF-κB 和 PPARγmRNA 的錶達。結果與模型組相比,噹歸芍藥散組小鼠血清 TC 和 LDL-C 水平明顯降低(P<0.01),肝髒組織中 NF-κB mRNA 的錶達降低,差異有統計學意義(P<0.05),PPARγmRNA 的錶達提高,差異有統計學意義(P<0.05)。結論噹歸芍藥散可降低代謝性炎性反應小鼠血脂和血清炎性反應因子 IL-6和 MCP-1濃度,併可通過調控覈轉錄因子 NF-κB 和 PPARγ受體,抑製小鼠體內代謝性炎性反應,從而可能對早期動脈粥樣硬化起到榦預作用。
목적:연구당귀작약산대대사성염성반응소서혈지화혈청염성반응인자백세포개소-6(interleukin-6,IL-6)、단핵세포추화단백-1(monocyte chemotactic protein 1,MCP-1)이급핵인자κB (nuclear factor kappa B,NF-κB)화활화적과양화물매체증생물격활수체γ(peroxisome proliferator-activated receptor gamma,PPARγ)mRNA 표체적영향。방법60지웅성 C57소서,채용수자표법장동물수궤분위정상조、모형조、립보타조、당귀작약산조(n =15)。채용고지음식연합지다당주사조성소서대사성염성반응모형。조모5주후,개시관위급약,매천2차,당귀작약산2.2 g/ kg,립보타0.003 g/ kg。정상대조조화모형조관복등체적증류수。련속관위5주。처사후채혈화취간장,검측각조소서혈청담고순(total cholesterol,TC)、삼선감유(triglyceride,TG)화저밀도지단백담고순(low density lipoprotein,LDL-C)농도,병채용류식세포술검측혈청염성반응인자 IL-6화 MCP-1농도。반전록취합매련식반응(reverse transcription polymerase chain reaction,RT-PCR)법측정간장 NF-κB 화 PPARγmRNA 적표체。결과여모형조상비,당귀작약산조소서혈청 TC 화 LDL-C 수평명현강저(P<0.01),간장조직중 NF-κB mRNA 적표체강저,차이유통계학의의(P<0.05),PPARγmRNA 적표체제고,차이유통계학의의(P<0.05)。결론당귀작약산가강저대사성염성반응소서혈지화혈청염성반응인자 IL-6화 MCP-1농도,병가통과조공핵전록인자 NF-κB 화 PPARγ수체,억제소서체내대사성염성반응,종이가능대조기동맥죽양경화기도간예작용。
Objective To study the effect of Dangguishaoyaosan on the blood lipids and the expression of inflammatory factors, such as IL-6, MCP-1, NF-κB and PPAR-γ mRNA in the metaflammatory mice. Methods Sixty male C57 mice were randomly divided into normal group, model group, the lipitor group and Dangguishaoyaosan group(n = 15). High-fat diets joining lipopolysaccharide injection were used to build the metabolic inflammatory model in mice. Five weeks later, all groups in addition to the normal were given a gavage twice a day for five weeks,according to the dose conversed from the clinical equivalent dose. When the test was finished, we collect the blood and liver, test the serum cholesterol( TC), triglyceride( TG) and low density lipoprotein cholesterol( LDL-C) level, using flow cytometry to detect the serum level of IL-6 and MCP-1. Reverse transcription polymerase chain reaction(RT-PCR) was used to detect the expression of NF-κB and PPAR-γ mRNA in liver. Results Compared with the model group, the serum TC and LDL-C level of Dangguishaoyaosan group significantly decreased(P<0. 01), and the expression of NF-κB mRNA in liver tissue decreased significantly(P<0. 01), while the expression of PPAR-γmRNA significantly increased(P<0. 01). Conclusion Dangguishaoyaosan can reduce the blood lipid, IL-6 and MCP-1 level of metabolic inflammation mice, and can influence metabolic inflammation in mice, which might have an intervention effect on the early atherosclerosis through regulating nuclear transcription factor NF-κB and PPAR-γ receptors.