中国全科医学
中國全科醫學
중국전과의학
Chinese General Practice
2015年
27期
3314-3319
,共6页
紫外线%藏雪莲多糖%皮肤角质形成细胞%白细胞介素6%肿瘤坏死因子α%丝裂原激活蛋白激酶类%淋巴瘤,B细胞%Bcl-2相关X蛋白质%半胱氨酸蛋白酶类
紫外線%藏雪蓮多糖%皮膚角質形成細胞%白細胞介素6%腫瘤壞死因子α%絲裂原激活蛋白激酶類%淋巴瘤,B細胞%Bcl-2相關X蛋白質%半胱氨痠蛋白酶類
자외선%장설련다당%피부각질형성세포%백세포개소6%종류배사인자α%사렬원격활단백격매류%림파류,B세포%Bcl-2상관X단백질%반광안산단백매류
Ultraviolet rays%Saussurea Tridactyla Sch. - Bip. polysaccharides%HaCaT cells%Interleukin -6%Tumor necrosis factor - alpha%Mitogen - activated protein kinases%Lymphoma,B - cell%Bcl-2 - associated X protein%Cysteine proteases
目的:探讨藏雪莲(SSB)多糖是否通过P38丝裂原激活蛋白激酶(P38MAPK)通路减轻中波紫外线( UVB)辐射后皮肤角质形成细胞( HaCaT细胞)凋亡引起炎性损伤。方法2014年10月—2015年3月,提取SSB多糖,体外培养 HaCaT 细胞,将 HaCaT 细胞分为低剂量辐射组(30 mJ/cm2,辐射1 h, A 组)和高剂量辐射组(60 mJ/cm2,辐射1 h,B组);将A组和B组又分别分为对照组(1组)、辐射组( UVB,2组)、低剂量SSB多糖组(UVB+SSB 10 mg/ml,3组)和高剂量SSB多糖组(UVB+SSB 40 mg/ml,4组)。采用酶联免疫吸附实验(ELISA)法检测并比较白介素6(IL-6)、肿瘤坏死因子α(TNF -α)、P38MAPK、P53、B 细胞淋巴瘤因子2(Bcl-2)、Bcl-2相关X(Bax)、半胱氨酸蛋白酶3(Caspase -3)水平。结果 A2组IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3水平高于A1组,Bcl-2水平低于A1组(P<0.05);A3组IL-6、TNF-α、P38MAPK、Caspase-3水平高于A1组(P<0.05);A4组TNF-α、Bcl-2水平高于A1组(P<0.05);A3组、A4组IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3水平低于A2组,Bcl-2水平高于A2组(P<0.05);A4组IL-6、TNF-α、Caspase-3水平低于A3组,Bcl-2水平高于A3组(P<0.05)。B2组IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3水平高于B1组,Bcl-2水平低于B1组(P<0.05);B3组IL-6、TNF-α水平高于B1组,Bcl-2水平低于B1组(P<0.05);B4组IL-6、Bcl-2水平高于B1组, TNF -α、Caspase -3水平低于 B1组( P <0.05);B3组、B4组IL-6、TNF -α、P38MAPK、P53、Bax、Caspase-3水平低于 B2组,Bcl-2水平高于 B2组(P <0.05);B4组IL-6、TNF -α、Caspase-3水平低于B3组,Bcl-2水平高于B3组(P<0.05)。结论 SSB多糖通过P38MAPK通路减少UVB辐射后HaCaT细胞凋亡,进而减轻HaCaT细胞的炎性损伤。
目的:探討藏雪蓮(SSB)多糖是否通過P38絲裂原激活蛋白激酶(P38MAPK)通路減輕中波紫外線( UVB)輻射後皮膚角質形成細胞( HaCaT細胞)凋亡引起炎性損傷。方法2014年10月—2015年3月,提取SSB多糖,體外培養 HaCaT 細胞,將 HaCaT 細胞分為低劑量輻射組(30 mJ/cm2,輻射1 h, A 組)和高劑量輻射組(60 mJ/cm2,輻射1 h,B組);將A組和B組又分彆分為對照組(1組)、輻射組( UVB,2組)、低劑量SSB多糖組(UVB+SSB 10 mg/ml,3組)和高劑量SSB多糖組(UVB+SSB 40 mg/ml,4組)。採用酶聯免疫吸附實驗(ELISA)法檢測併比較白介素6(IL-6)、腫瘤壞死因子α(TNF -α)、P38MAPK、P53、B 細胞淋巴瘤因子2(Bcl-2)、Bcl-2相關X(Bax)、半胱氨痠蛋白酶3(Caspase -3)水平。結果 A2組IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3水平高于A1組,Bcl-2水平低于A1組(P<0.05);A3組IL-6、TNF-α、P38MAPK、Caspase-3水平高于A1組(P<0.05);A4組TNF-α、Bcl-2水平高于A1組(P<0.05);A3組、A4組IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3水平低于A2組,Bcl-2水平高于A2組(P<0.05);A4組IL-6、TNF-α、Caspase-3水平低于A3組,Bcl-2水平高于A3組(P<0.05)。B2組IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3水平高于B1組,Bcl-2水平低于B1組(P<0.05);B3組IL-6、TNF-α水平高于B1組,Bcl-2水平低于B1組(P<0.05);B4組IL-6、Bcl-2水平高于B1組, TNF -α、Caspase -3水平低于 B1組( P <0.05);B3組、B4組IL-6、TNF -α、P38MAPK、P53、Bax、Caspase-3水平低于 B2組,Bcl-2水平高于 B2組(P <0.05);B4組IL-6、TNF -α、Caspase-3水平低于B3組,Bcl-2水平高于B3組(P<0.05)。結論 SSB多糖通過P38MAPK通路減少UVB輻射後HaCaT細胞凋亡,進而減輕HaCaT細胞的炎性損傷。
목적:탐토장설련(SSB)다당시부통과P38사렬원격활단백격매(P38MAPK)통로감경중파자외선( UVB)복사후피부각질형성세포( HaCaT세포)조망인기염성손상。방법2014년10월—2015년3월,제취SSB다당,체외배양 HaCaT 세포,장 HaCaT 세포분위저제량복사조(30 mJ/cm2,복사1 h, A 조)화고제량복사조(60 mJ/cm2,복사1 h,B조);장A조화B조우분별분위대조조(1조)、복사조( UVB,2조)、저제량SSB다당조(UVB+SSB 10 mg/ml,3조)화고제량SSB다당조(UVB+SSB 40 mg/ml,4조)。채용매련면역흡부실험(ELISA)법검측병비교백개소6(IL-6)、종류배사인자α(TNF -α)、P38MAPK、P53、B 세포림파류인자2(Bcl-2)、Bcl-2상관X(Bax)、반광안산단백매3(Caspase -3)수평。결과 A2조IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3수평고우A1조,Bcl-2수평저우A1조(P<0.05);A3조IL-6、TNF-α、P38MAPK、Caspase-3수평고우A1조(P<0.05);A4조TNF-α、Bcl-2수평고우A1조(P<0.05);A3조、A4조IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3수평저우A2조,Bcl-2수평고우A2조(P<0.05);A4조IL-6、TNF-α、Caspase-3수평저우A3조,Bcl-2수평고우A3조(P<0.05)。B2조IL-6、TNF-α、P38MAPK、P53、Bax、Caspase-3수평고우B1조,Bcl-2수평저우B1조(P<0.05);B3조IL-6、TNF-α수평고우B1조,Bcl-2수평저우B1조(P<0.05);B4조IL-6、Bcl-2수평고우B1조, TNF -α、Caspase -3수평저우 B1조( P <0.05);B3조、B4조IL-6、TNF -α、P38MAPK、P53、Bax、Caspase-3수평저우 B2조,Bcl-2수평고우 B2조(P <0.05);B4조IL-6、TNF -α、Caspase-3수평저우B3조,Bcl-2수평고우B3조(P<0.05)。결론 SSB다당통과P38MAPK통로감소UVB복사후HaCaT세포조망,진이감경HaCaT세포적염성손상。
Objective To investigate whether Saussurea Tridactyla Sch. - Bip. ( SSB ) polysaccharides could alleviate inflammatory damage induced by the apoptosis of HaCaT cells after ultraviolet B( UVB) radiation through P38MAPK passage. Methods From October 2014 to March 2015,SSB polysaccharideswere extracted,and HaCaT cells were cultured in vitro and were respectively divided into low dose radiation group(30 mJ/cm2 ,radiation 1 h,group A),high dose radiation group (60 mJ/cm2,radiation 1 h,group B). Each of the two groups were further divided into control group(group 1),UVB radiation group(UVB,group 2),low dose SSB polysaccharide group(UVB+SSB 10 mg/ml,group 3),high dose SSB polysaccharide group(UVB+SSB 40 mg/ml,group 4). ELISA method was used to test and compare the levels of IL-6,TNF-α,P38MAPK, P53,Bcl-2,Bax and Caspase-3. Results Group A2 was higher(P<0. 05)in the levels of IL-6,TNF-α,P38MAPK, P53,Bax and Caspase-3 and lower(P<0. 05)in the level of Bcl-2 than group A1;group A3 was higher(P<0. 05)than group A1 in the levels of IL-6,TNF-α,P38MAPK and Caspase-3;group A4 was higher(P<0. 05)than group A1 in the levels of TNF-α and Bcl-2;group A3 and group A4 were lower(P<0. 05)in the levels of IL-6,TNF-α,P38MAPK, P53,Bax and Caspase-3 and higher(P<0. 05)in the level of Bcl-2 than group A2;group A4 was lower(P<0. 05)in the levels of IL-6,TNF-αand Caspase-3 and higher(P<0. 05)in the level of Bcl-2 than group A3. Group B2 was higher(P<0. 05)in the levels of IL-6,TNF-α,P38MAPK,P53,Bax and Caspase-3 and lower(P<0. 05)in the level of Bcl-2 than group B1;group B3 was higher(P<0. 05)in the levels of IL-6 and TNF-αand lower(P<0. 05)in the level of Bcl-2 than group B1;group B4 was higher(P<0. 05)in the levels of IL-6 and Bcl-2 and lower(P<0. 05)in the level of TNF-αand Caspase-3 than group B1;group B3 and group B4 were lower(P<0. 05)in the levels of IL-6,TNF-α,P38MAPK, P53,Bax and Caspase-3 and higher(P<0. 05)in the level of Bcl-2 than group B2;group B4 was lower(P<0. 05)in the levels of IL-6,TNF -α and Caspase -3 and higher(P <0. 05)in the level of Bcl-2 than group B3. Conclusion SSB polysaccharides could alleviate inflammatory damage induced by the apoptosis of HaCaT cells after UVB radiation through P38MAPK passage.