世界中医药
世界中醫藥
세계중의약
WORLD CHINESE MEDICINE
2015年
1期
86-88
,共3页
王杰%张文斌%牟界%雷文汇%李芹
王傑%張文斌%牟界%雷文彙%李芹
왕걸%장문빈%모계%뢰문회%리근
松针%呼吸道合胞病毒感染%TLR3%TLR4
鬆針%呼吸道閤胞病毒感染%TLR3%TLR4
송침%호흡도합포병독감염%TLR3%TLR4
Pine needles%Respiratory syncytial virus infection%TLR3%TLR4%Protein
目的:通过观察松针对呼吸道合胞病毒感染小鼠肺组织Toll样受体3(TLR3)及Toll样受体4(TLR4)蛋白表达的影响,探讨其治疗呼吸道合胞病毒感染的可能免疫调节机制。方法:采用美国癌症研究所( Institute of Cancer Research)培育的ICR小鼠60只随机分为6组:正常对照组、模型组、利巴韦林组、松针高剂量组、中剂量组呼、低剂量组,呼吸道合胞病毒滴鼻后给药,观察肺组织TLR3及TLR4蛋白的表达。结果:松针高剂量组可降低小鼠肺组织TLR3及TLR4蛋白的表达,与模型组比较差异有统计学意义( P<0.05)。结论:松针可抑制呼吸道合胞病毒感染小鼠肺组织中TLR3及TLR4蛋白的表达,可能为其免疫调节作用的机制之一。
目的:通過觀察鬆針對呼吸道閤胞病毒感染小鼠肺組織Toll樣受體3(TLR3)及Toll樣受體4(TLR4)蛋白錶達的影響,探討其治療呼吸道閤胞病毒感染的可能免疫調節機製。方法:採用美國癌癥研究所( Institute of Cancer Research)培育的ICR小鼠60隻隨機分為6組:正常對照組、模型組、利巴韋林組、鬆針高劑量組、中劑量組呼、低劑量組,呼吸道閤胞病毒滴鼻後給藥,觀察肺組織TLR3及TLR4蛋白的錶達。結果:鬆針高劑量組可降低小鼠肺組織TLR3及TLR4蛋白的錶達,與模型組比較差異有統計學意義( P<0.05)。結論:鬆針可抑製呼吸道閤胞病毒感染小鼠肺組織中TLR3及TLR4蛋白的錶達,可能為其免疫調節作用的機製之一。
목적:통과관찰송침대호흡도합포병독감염소서폐조직Toll양수체3(TLR3)급Toll양수체4(TLR4)단백표체적영향,탐토기치료호흡도합포병독감염적가능면역조절궤제。방법:채용미국암증연구소( Institute of Cancer Research)배육적ICR소서60지수궤분위6조:정상대조조、모형조、리파위림조、송침고제량조、중제량조호、저제량조,호흡도합포병독적비후급약,관찰폐조직TLR3급TLR4단백적표체。결과:송침고제량조가강저소서폐조직TLR3급TLR4단백적표체,여모형조비교차이유통계학의의( P<0.05)。결론:송침가억제호흡도합포병독감염소서폐조직중TLR3급TLR4단백적표체,가능위기면역조절작용적궤제지일。
Objective:To observe the effect of pine in respiratory syncytial virus infection in the expression of TLR3 lung tissue and TLR4 protein in mice,and explore the immune regulation mechanism of the treatment of respiratory syncytial virus infection. Methods:60 ICR mice were randomly divided into 5 groups: normal control group,model group,the antiviral oral liquid group, ribavirin,and pine needles.After intranasal administration of respiratory syncytial virus,observe TLR3 lung tissue and the expres-sion of TLR4 protein.Results:The antiviral oral liquid,ribavirin,pine needles can reduce the TLR3 and the expression of TLR4 protein of lung tissue in mice,compared with model group with significant difference ( P<0.05) .Conclusion: Pine needles can inhibit the respiratory syncytial virus infection in the lung tissue of mice TLR3 and the expression of TLR4 protein,and may be one of the mechanisms of immune regulation.