苦参素%肝炎,乙型,慢性%受体,抗原,T细胞%T淋巴细胞,细胞毒性
苦參素%肝炎,乙型,慢性%受體,抗原,T細胞%T淋巴細胞,細胞毒性
고삼소%간염,을형,만성%수체,항원,T세포%T림파세포,세포독성
Kurarinol%Hepatitis B,chronic%Receptors,antigen,T-cell%T Lymphocytes,cytotoxic
目的 通过研究苦参素对慢性乙型肝炎(CHB)患者细胞毒性T淋巴细胞(CTL)表面程序性死亡受体-1(PD-1)表达的影响,探讨苦参素抗病毒的机制.方法 69例CHB患者,HBV DNA≥104拷贝/ml,HBeAg阳性,人白细胞抗原(HLA)-A2阳性,丙氨酸转氨酶(ALT) ＞2×正常值上限(ULN),69例随机分为二组:治疗组34例,用苦参素葡萄糖注射液600 mg,静脉滴注,每日1次,1个月后改为苦参素胶囊200 mg口服,每日3次,水飞蓟宾葡甲胺片200 mg口服,每日3次,对照组35例,只用水飞蓟宾葡甲胺片,用法用量同治疗组.分析比较3个月后患者的外周血HBV特异性CTL表面PD-1表达、非特异性CTL表面PD-1表达和HBV特异性CTL水平,HBV DNA和HBeAg阴转率及肝功能.结果 治疗3个月后,治疗组外周血HBV特异性CTL表面PD-1表达较治疗前下降(t=2.39,P＜0.05),也较对照组治疗后3个月下降(t=2.26,P＜0.05),HBV特异性CTL水平较治疗前升高(t =3.01,P＜0.01),也较对照组治疗后升高(t=2.65,P＜0.05).非特异性CTL表面PD-1表达与治疗前比较,差别无统计学意义(P＞0.05),与对照组治疗后比较,差别无统计学意义(P＞0.05).HBV DNA阴转(HBV DNA ＜500拷贝/ml)11例(32.35％),高于对照组治疗后(2例,占5.71％)x2 =7.99,P＜0.01,HBeAg阴转9例(26.47％),高于对照组治疗后(1例,占2.86％),x2=7.75,P＜0.01.结论 苦参素通过下调CHB患者外周血HBV特异性CTL表面PD-1表达,提高HBV特异性CTL水平,是苦参素清除或抑制CHB患者HBV的可能机制之一.
目的 通過研究苦參素對慢性乙型肝炎(CHB)患者細胞毒性T淋巴細胞(CTL)錶麵程序性死亡受體-1(PD-1)錶達的影響,探討苦參素抗病毒的機製.方法 69例CHB患者,HBV DNA≥104拷貝/ml,HBeAg暘性,人白細胞抗原(HLA)-A2暘性,丙氨痠轉氨酶(ALT) ＞2×正常值上限(ULN),69例隨機分為二組:治療組34例,用苦參素葡萄糖註射液600 mg,靜脈滴註,每日1次,1箇月後改為苦參素膠囊200 mg口服,每日3次,水飛薊賓葡甲胺片200 mg口服,每日3次,對照組35例,隻用水飛薊賓葡甲胺片,用法用量同治療組.分析比較3箇月後患者的外週血HBV特異性CTL錶麵PD-1錶達、非特異性CTL錶麵PD-1錶達和HBV特異性CTL水平,HBV DNA和HBeAg陰轉率及肝功能.結果 治療3箇月後,治療組外週血HBV特異性CTL錶麵PD-1錶達較治療前下降(t=2.39,P＜0.05),也較對照組治療後3箇月下降(t=2.26,P＜0.05),HBV特異性CTL水平較治療前升高(t =3.01,P＜0.01),也較對照組治療後升高(t=2.65,P＜0.05).非特異性CTL錶麵PD-1錶達與治療前比較,差彆無統計學意義(P＞0.05),與對照組治療後比較,差彆無統計學意義(P＞0.05).HBV DNA陰轉(HBV DNA ＜500拷貝/ml)11例(32.35％),高于對照組治療後(2例,佔5.71％)x2 =7.99,P＜0.01,HBeAg陰轉9例(26.47％),高于對照組治療後(1例,佔2.86％),x2=7.75,P＜0.01.結論 苦參素通過下調CHB患者外週血HBV特異性CTL錶麵PD-1錶達,提高HBV特異性CTL水平,是苦參素清除或抑製CHB患者HBV的可能機製之一.
목적 통과연구고삼소대만성을형간염(CHB)환자세포독성T림파세포(CTL)표면정서성사망수체-1(PD-1)표체적영향,탐토고삼소항병독적궤제.방법 69례CHB환자,HBV DNA≥104고패/ml,HBeAg양성,인백세포항원(HLA)-A2양성,병안산전안매(ALT) ＞2×정상치상한(ULN),69례수궤분위이조:치료조34례,용고삼소포도당주사액600 mg,정맥적주,매일1차,1개월후개위고삼소효낭200 mg구복,매일3차,수비계빈포갑알편200 mg구복,매일3차,대조조35례,지용수비계빈포갑알편,용법용량동치료조.분석비교3개월후환자적외주혈HBV특이성CTL표면PD-1표체、비특이성CTL표면PD-1표체화HBV특이성CTL수평,HBV DNA화HBeAg음전솔급간공능.결과 치료3개월후,치료조외주혈HBV특이성CTL표면PD-1표체교치료전하강(t=2.39,P＜0.05),야교대조조치료후3개월하강(t=2.26,P＜0.05),HBV특이성CTL수평교치료전승고(t =3.01,P＜0.01),야교대조조치료후승고(t=2.65,P＜0.05).비특이성CTL표면PD-1표체여치료전비교,차별무통계학의의(P＞0.05),여대조조치료후비교,차별무통계학의의(P＞0.05).HBV DNA음전(HBV DNA ＜500고패/ml)11례(32.35％),고우대조조치료후(2례,점5.71％)x2 =7.99,P＜0.01,HBeAg음전9례(26.47％),고우대조조치료후(1례,점2.86％),x2=7.75,P＜0.01.결론 고삼소통과하조CHB환자외주혈HBV특이성CTL표면PD-1표체,제고HBV특이성CTL수평,시고삼소청제혹억제CHB환자HBV적가능궤제지일.
Objective To explore the anti-viral mechanism of kurarinol through studying its influence on cytotoxic T lymphocyte (CTL) surface program death receptor-1 (PD-1) expression of patients with chronic hepatitis B (CHB).Methods 69 cases of CHB,HBV DNA ≥ 104 copies/ml,HBeAg positive,human leukocyte antigen (HLA)-A2 positive,alanine aminotransferase (ALT) ＞ 2 × upper limit of normal value(ULN).69 cases were randomly divided into two groups:34 cases in treatment group,600 mg of kurarinol glucose injection was used for intravenous dripping,once a day,one month later,200 mg of kurarinol capsule was used orally,three times a day and.200 mg of silybin meglumine tablet was used orally,three times a day.35 cases in control group,only silibin meglumine tablet was used,method and dosage were the same as those of treatment group.Three months later,their peripheral blood HBV specific CTL surface PD-1 expression,non-specific CTL surface PD-1 expression and level of HBV specific CTL,HBV DNA and HBeAg negative rate and liver functions were analyzed and compared.Results 3 months after treatment,peripheral blood HBV specific CTL surface PD-1 expression of the treatment group decreased compared with that before treatment(t =2.39,P ＜ 0.05),it also decreased compared with that of the control group 3 months after treatment(t =2.26,P ＜ 0.05),HBV specific CTL increased compared with that before treatment(t =3.01,P ＜ 0.01),it also increased compared with that of the control group after treatment (t =2.65,P ＜0.05).There was no significant difference of non-specific CTL surface PD-1 expression compared with that before treatment(P ＞ 0.05),and there was no significant difference compared with that of the control group after treatment(P ＞ 0.05).HBV DNA of 11 cases (32.5％) turned negative (HBV DNA ＜ 500 copies/ml),higher than that of the control group after treatment(2 cases,5.71％)x2 =7.99,P ＜ 0.01,H BeAg of 9 cases(26.47％) turned negative,higher than that of the control group after treatment(1 case,2.86％),x2 =7.75,P ＜ 0.01.Conclusion Kurarinol can increase level of HBV specific CTL by down-regulating peripheral blood HBV specific CTL surface PD-1 expression of CHB patients,which may be one of the possible mechanisms that kurarinol can remove or inhibit HBV of CHB patients.
