Background:Chronic pain is defined as pain that lasts for three months or even more.Over 25%of the global population suffers from chronic pain.Tong-luo Qu-tong(TLQT)Plaster is clinically used to treat arthritis.Howeve...Background:Chronic pain is defined as pain that lasts for three months or even more.Over 25%of the global population suffers from chronic pain.Tong-luo Qu-tong(TLQT)Plaster is clinically used to treat arthritis.However,its ability to treat chronic pain remains largely unknown.Methods:In this study,we explored the molecular mechanism of TLQT plaster in relieving chronic muscle pain by combining network pharmacology and RNA-seq analysis.We also applied the Elisa and the RT-qPCR.Results:We found 447 targets in TLQT and 13,599 targets related to chronic pain disease.And 419 intersecting targets were obtained,which mainly enrich the IL-17 signaling pathway,TNF signaling pathway,and Th17 cell differentiation pathway.Further,we constructed the SD rat model of chronic pain.The results of Von Frey Hair Test showed that the relief of muscle pain TLQT treated group was twice as much as that in the model group.The hot plate test results showed that the time of lifting the foot was 1.3 times as much as that of the model group.Moreover,TLQT effectively reduced the inflammation in rat muscle.With RNA-seq analysis,230 differentially expressed genes were collected.The RT-qPCR results indicated that the mRNA expression level of NCF1,CXCL10,and ICAM1 all promoted in the model group,and then decreased significantly in the TLQT treated group.The ELISA results performed that the level of IL-1βand IL-6 in TLQT group high dose group was reduced by about 1.6-fold,and for TNF-α,it was reduced by about 2.6-fold compared with the model group.Immunohistochemistry assay showed that the expression level of CXCL10 and ICAM1 was both up-regulated in the model group and down-regulated in the TLQT group.Conclusion:TLQT plaster reduces chronic muscle pain by inhibiting the expression of NCF1,CXCL10,and ICAM1 and reducing the level of muscle tissue inflammation.展开更多
文摘Background:Chronic pain is defined as pain that lasts for three months or even more.Over 25%of the global population suffers from chronic pain.Tong-luo Qu-tong(TLQT)Plaster is clinically used to treat arthritis.However,its ability to treat chronic pain remains largely unknown.Methods:In this study,we explored the molecular mechanism of TLQT plaster in relieving chronic muscle pain by combining network pharmacology and RNA-seq analysis.We also applied the Elisa and the RT-qPCR.Results:We found 447 targets in TLQT and 13,599 targets related to chronic pain disease.And 419 intersecting targets were obtained,which mainly enrich the IL-17 signaling pathway,TNF signaling pathway,and Th17 cell differentiation pathway.Further,we constructed the SD rat model of chronic pain.The results of Von Frey Hair Test showed that the relief of muscle pain TLQT treated group was twice as much as that in the model group.The hot plate test results showed that the time of lifting the foot was 1.3 times as much as that of the model group.Moreover,TLQT effectively reduced the inflammation in rat muscle.With RNA-seq analysis,230 differentially expressed genes were collected.The RT-qPCR results indicated that the mRNA expression level of NCF1,CXCL10,and ICAM1 all promoted in the model group,and then decreased significantly in the TLQT treated group.The ELISA results performed that the level of IL-1βand IL-6 in TLQT group high dose group was reduced by about 1.6-fold,and for TNF-α,it was reduced by about 2.6-fold compared with the model group.Immunohistochemistry assay showed that the expression level of CXCL10 and ICAM1 was both up-regulated in the model group and down-regulated in the TLQT group.Conclusion:TLQT plaster reduces chronic muscle pain by inhibiting the expression of NCF1,CXCL10,and ICAM1 and reducing the level of muscle tissue inflammation.
文摘目的研究CXCL10血清水平及单核苷酸多态性(single nucleotide polymorphisms,SNPs)与未接受干扰素(interferon,IFN)α治疗的慢性丙型肝炎(chronic hepatitis C,CHC)患者发生甲状腺功能异常的相关性。方法在前期已经进行甲状腺功能检测的312例未接受IFNα治疗的CHC患者中,筛选出与发生甲状腺功能异常的39例患者(甲状腺功能异常组)匹配的甲状腺功能正常患者39例(甲状腺功能正常组)。采用ELISA分别检测2组血清CXCL10水平;采用QIAamp DNA Blood Mini Kit提取2组患者基因组DNA,分别对CXCL10-135和CXCL10-1447基因片段进行PCR扩增和直接序列测定,应用BioEdit软件对样本序列进行分析。结果甲状腺功能异常组和正常组的血清CXCL10水平分别为(472.11±274.91)pg/ml和(516.39±272.40)pg/ml,2组比较差异无统计学意义。甲状腺功能异常组CXCL10-135的G、T等位基因频率分别为95.0%和5.0%,甲状腺功能正常组的G、T等位基因频率分别为96.2%和3.8%,2组比较差异无统计学意义。甲状腺功能异常组CXCL10-1447的A、G等位基因频率分别为41.7%和58.3%,甲状腺功能正常组的A、G等位基因频率分别为47.4%和52.6%,2组比较差异无统计学意义。甲状腺功能异常组CXCL10-135的GG、GT、TT基因型频率分别为93.4%、3.3%和3.3%,甲状腺功能正常组的GG、GT、TT基因型频率分别为92.3%、7.7%和0%,2组比较差异无统计学意义。甲状腺功能异常组CXCL10-1447的AA、AG、GG基因型频率分别为16.7%、50.0%和33.3%,甲状腺功能正常组的AA、AG、GG基因型频率分别为20.5%、53.9%和25.6%,2组比较差异无统计学意义。结论未接受IFNα治疗的CHC患者发生甲状腺功能异常与CXCL10血清水平和基因多态性位点-135、-1447无相关性。
