中国麻风皮肤病杂志
中國痳風皮膚病雜誌
중국마풍피부병잡지
CHINA JOURNAL OF LEPROSY AND SKIN DISEASES
2014年
6期
327-330
,共4页
刘海平%高华%付洪军
劉海平%高華%付洪軍
류해평%고화%부홍군
人参皂苷Rb1%B16F10细胞%凋亡
人參皂苷Rb1%B16F10細胞%凋亡
인삼조감Rb1%B16F10세포%조망
ginsenoside Rb1%B16F10 cells%apoptosis
目的:确定人参皂苷Rb1对过氧化氢诱导的B16F10黑素瘤细胞凋亡的保护作用。方法:将B16F10细胞随机分为对照组,H2 O2组和Rb1+H2 O2组(细胞培养液中分别加入10 mg/L、20 mg/L、50 mg/L的人参皂苷Rb1和H2 O2)。分别测定B16F10细胞活力、LDH漏出量、线粒体膜电位及细胞凋亡水平。结果: H2O2作用24 h后,B16F10细胞活力降低至对照组的53.77%,而Annexin V和PI阳性细胞比例为25.6%,显著高于对照组( P<0.01)。50 mg/L人参皂苷Rb1预处理后,B16F10细胞活力为对照组的77.75%,较H2 O2组增加44.6%( P<0.01)。 Annexin V和PI阳性细胞比例为14.4%,明显低于H2 O2组( P<0.01),并且LDH漏出率明显降低,线粒体膜电位显著升高。结论:人参皂苷Rb1对H2 O2所致的B16F10黑素瘤细胞凋亡具有保护作用,有效提高其抗氧化应激能力。
目的:確定人參皂苷Rb1對過氧化氫誘導的B16F10黑素瘤細胞凋亡的保護作用。方法:將B16F10細胞隨機分為對照組,H2 O2組和Rb1+H2 O2組(細胞培養液中分彆加入10 mg/L、20 mg/L、50 mg/L的人參皂苷Rb1和H2 O2)。分彆測定B16F10細胞活力、LDH漏齣量、線粒體膜電位及細胞凋亡水平。結果: H2O2作用24 h後,B16F10細胞活力降低至對照組的53.77%,而Annexin V和PI暘性細胞比例為25.6%,顯著高于對照組( P<0.01)。50 mg/L人參皂苷Rb1預處理後,B16F10細胞活力為對照組的77.75%,較H2 O2組增加44.6%( P<0.01)。 Annexin V和PI暘性細胞比例為14.4%,明顯低于H2 O2組( P<0.01),併且LDH漏齣率明顯降低,線粒體膜電位顯著升高。結論:人參皂苷Rb1對H2 O2所緻的B16F10黑素瘤細胞凋亡具有保護作用,有效提高其抗氧化應激能力。
목적:학정인삼조감Rb1대과양화경유도적B16F10흑소류세포조망적보호작용。방법:장B16F10세포수궤분위대조조,H2 O2조화Rb1+H2 O2조(세포배양액중분별가입10 mg/L、20 mg/L、50 mg/L적인삼조감Rb1화H2 O2)。분별측정B16F10세포활력、LDH루출량、선립체막전위급세포조망수평。결과: H2O2작용24 h후,B16F10세포활력강저지대조조적53.77%,이Annexin V화PI양성세포비례위25.6%,현저고우대조조( P<0.01)。50 mg/L인삼조감Rb1예처리후,B16F10세포활력위대조조적77.75%,교H2 O2조증가44.6%( P<0.01)。 Annexin V화PI양성세포비례위14.4%,명현저우H2 O2조( P<0.01),병차LDH루출솔명현강저,선립체막전위현저승고。결론:인삼조감Rb1대H2 O2소치적B16F10흑소류세포조망구유보호작용,유효제고기항양화응격능력。
Objective: To determine the protective effects of ginsenoside Rb1 on B16F10 cells apoptosis induced by H2 O2 . Methods:B16F10 cells were randomly divided into blank control group H2 O2 group and Rb1+H2 O2 group. In the Rb1+H2 O2 group B16F10 cells were cultured with ginsenoside Rb1 ( in three doses of 10 mg/L 20 mg/L and 50mg/L) before treated with H2 O2 . The viability of B16F10 cells was calculated by MTT assay. The outleakage of lactate dehydrogenase ( LDH) mitochondrial membrane potential and the level of apoptosis were measured accordingly. Results: After treated with H2 O2 for 24h the viability of B16F10 cells decreased to 53.77% of the control group while the proportion of Annexin V&PI positive cells significantly increased to 25.6% of the control group ( P<0.01) . When pre-treated with 50 mg/L Rb1 the cell viability increased to 77.75% of the control group which was 44.6% higher than that of the H2O2 group (P<0.01) . The proportion of Annexin V&PI positive cells significantly decreased to 14.4% compared with H2 O2 group (P<0.01). Meanwhile ginsenoside Rb1 (50 mg/L) significantly decreased LDH outleakage and inhibited the decrease of mitochondrial membrane potential. Conclusion:Ginsenoside Rb1 can protect the B16F10 cells against H2 O2- induced apoptosis and effectively improve the ability of antioxidative stress.