The Experimental and Clinical Study on the Effect of Curcumin on Cell Cycle Proteins and Regulating Proteins of Apoptosis in Acute Myelogenous Leukemia

To investigate whether the Bcl- 2 gene family is involved in m odulating mechanism of apoptosis and change of cell cycle protein induced by curcumin in acute myeloid leukemia HL - 6 0 cell line and primary acute m yelogenous leukem ic cells,the Bcl- 2 family member Mcl- 1,Bax and Bak and cell cycle proteins including P2 7kipl,P2 1wafl,cyclin D3and p Rbp- were selected and their ex- pression detected by SABC imm uno- histochem ical stain m ethod.The attitude of sub- G1 peak in DNA histogram was determined by FCM.The TU NEL positive cell percentage was identified by term inal deoxynucleotidyl transferase (Td T ) - m ediated Biotin d U NP end labeling technique.It was found that when HL - 6 0 cells were treated with 2 5μm ol/ L curcumin for 2 4 h,the expression level of Mcl- 1was down- regulated,but that of Bax and Bak up- regulated time- dependently.There was significant difference in the expression level of Mcl- 1,Bax and Bak between the curcumin- treated groups and control group(P<0 .0 5 - 0 .0 1) .At the sam e time,curcumin had no effect on progress of cell cycle in prim aty acute m yelogenous leukemia at newly diagnosis,but could in- crease the peak of Sub- G1 (P<0 .0 5 ) ,and down- regulate the expression of Mcl- 1and up- regulate the expression of Bax and Bak with the difference being statistically significant.The expression of P2 7kipl,P2 1wafl and p Rbp- were elevated and thatof cyclin D3decreased in the presence of curcum in. These findings suggested thatthe Bcl- 2 gene fam ily indeed participated in the regulatory process of apoptosis induced by curcumin in HL - 6 0 cells and AML cells.Curcumin can induce apoptosis of primary acute myelogenous leukemic cells and disturb cell cycle progression of HL - 6 0 cells.The m echanism appeared to be m ediated by perturbing G0 / G1 phases checkpoints which associated with up- regulation of P2 7kipl,P2 1wafl and p Rbp- expression,and down- regulation of cyclin D3.

TiO_(2)-coated LiNi_(0.)9Co_(0.08)Al_(0.02)O_(2)cathode materials with enhanced cycle performance for Li-ion batteries

Ni-rich cathode material is one of the most promising materials for Li-ion batteries in electric vehicles.However,fading capacity,poor cyclic stability and high p H value are still major challenges,which suppress its practical application.In this study,spherical LiNi_(0.)9Co_(0.08)Al_(0.02)O_(2)powders with 0.4 wt%TiO_(2)coating layer were prepared by impregnation-hydrolysis method.Scanning electron microscopy(SEM),high-resolution transmission electron microscopy(HRTEM)and X-ray diffraction(XRD)results show that TiO_(2)is uniformly coated on the surface of LiNi_(0.)9Co_(0.08)Al_(0.02)O_(2)particle and slightly embedded into LiNi_(0.)9Co_(0.08)Al_(0.02)O_(2)particles.After 100 cycles at 2.0 C,0.4 wt%TiO_(2)-coated LiNi_(0.)9Co_(0.08)Al_(0.02)O_(2)electrode delivers much higher discharge capacity retention(77.0%)than the pristine LiNi_(0.)9Co_(0.08)Al_(0.02)O_(2)electrode(63.3%).The excellent cycling performance of 0.4 wt%Ti O_(2)-coated LiNi_(0.)9Co_(0.08)Al_(0.02)O_(2)electrode at a high discharge ratio is due to a TiO_(2)coating layer which can effectively reduce the direct contact between cathode material and electrolyte,suppress the oxidation of electrolyte,improve electrical conductivity of the electrode and increase the stability of the structure.

4’-去甲峨参内酯对四种肿瘤细胞凋亡的作用及机理研究

目的:探讨4’-去甲峨参内酯(0号衍生物)作用于Hela、MG-63、Hep G2、A549四种肿瘤细胞后,对Bcl-2、Bax基因表达、细胞周期及凋亡产生的影响。方法以0号衍生物作为观察组,0.1%DMSO作为空白对照组,紫杉醇作为阳性对照组,分别作用48 h后采用ELISA试剂盒检测对四种肿瘤细胞Bcl-2、Bax表达的影响;采用流式细胞仪PI单标法检测细胞周期进程及凋亡的影响。结果 ELISA试剂盒检测表明,观察组及阳性对照组与空白对照组比较Bcl-2/Bax比值均明显降低,具有显著性差异(P<0.05);流式细胞仪检测0号衍生物作用四种肿瘤细胞48h后对细胞周期进程及凋亡的影响,结果表明G0/G1期细胞百分数降低,G2/M期细胞百分数基本不变,而S期细胞百分数上升,说明0号衍生物阻滞肿瘤细胞于S期,且sub-G1细胞亚二倍体凋亡峰增加,进一步说明其诱导凋亡的作用。结论 0号衍生物通过上调Bax、下调Bcl-2,促进肿瘤细胞凋亡;阻滞肿瘤细胞于S期,sub-G1峰增加,显示其具有诱导细胞凋亡的作用。

基于JAK2/STAT3信号通路探讨芪苓白头翁汤对弥漫大B细胞淋巴瘤细胞增殖和凋亡的影响

目的:探讨芪苓白头翁汤对弥漫大B细胞淋巴瘤(DLBCL)细胞增殖、凋亡、非受体型酪氨酸蛋白激酶2/信号转导及转录激活因子3(JAK2/STAT3)信号通路及炎症因子白细胞介素^(-1)0(IL^(-1)0)的影响。方法:以人DLBCL细胞OCI-LY10、U2932细胞为研究对象,细胞增殖与活性检测法(CCK-8)检测细胞增殖情况,并计算出0、4.6、9.3、18.7、37.5、75、150 mg·L^(-1)芪苓白头翁汤处理OCI-LY10、U2932细胞24 h后的半抑制浓度(IC_(50))分别为9.33、16.13 mg·L^(-1)。后续相关实验根据芪苓白头翁汤作用于OCI-LY10、U2932细胞24 h半抑制浓度(IC_(50)),选用芪苓白头翁汤9.5、19、38 mg·L^(-1)开展实验。用胱天蛋白酶(Caspase)-3、Caspase-8、Caspase-9酶原活化检测试剂盒检测经0、9.5、19、38 mg·L^(-1)芪苓白头翁汤处理OCI-LY10、U2932细胞24 h后OCI-LY10、U2932细胞中Caspase-3、Caspase-8、Caspase-9的酶原活化情况。酶联免疫吸附测定法(ELISA)检测经0、9.5、19、38 mg·L^(-1)芪苓白头翁汤处理OCI-LY10、U2932细胞24 h后OCI-LY10、U2932细胞中IL^(-1)0炎症因子表达情况。流式细胞仪检测不同浓度芪苓白头翁汤作用OCI-LY10、U2932细胞24 h后细胞凋亡率及细胞周期。蛋白免疫印迹法(Western blot)检测0、9.5、19、38 mg·L^(-1)芪苓白头翁汤作用OCI-LY10、U2932细胞24 h,OCI-LY10、U2932细胞中B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、活化的聚腺苷二磷酸核糖聚合酶(cleaved PARP)、活化的Caspase-3(cleaved Caspase-3)凋亡蛋白表达情况及JAK2、STAT3、磷酸化(p)-JAK2、p-STAT3通路蛋白表达情况,不同浓度药物作用OCI-LY10、U2932细胞24 h,OCI-LY10、U2932细胞中癌基因(c-Myc)蛋白表达情况。结果:芪苓白头翁汤作用于OCI-LY10、U2932细胞24 h,与空白组比较,芪苓白头翁汤各组细胞增殖均受到明显抑制(P<0.05,P<0.01);9.5、19、38 mg·L^(-1)芪苓白头翁汤组Caspase-3、Caspase-8、Caspase-9酶原显著活化(P<0.01),细胞凋亡增加(P<0.05,P<0.01),细胞于DNA合成前期(G1)阻滞增加(P<0.05,P<0.01);9.5、19、38 mg·L^(-1)芪苓白头翁汤组OCI-LY10、U2932细胞中Bcl-2、p-JAK2、p-STAT3蛋白表达显著降低(P<0.01),Bax、cleaved PARP、cleaved Caspase-3蛋白表达显著增加(P<0.01),JAK2、STAT3蛋白表达未见明显改变。与空白组比较,19 mg·L^(-1)芪苓白头翁汤组、19 mg·L^(-1)芪苓白头翁汤+10μg·L^(-1)IL^(-1)0组c-Myc、p-JAK2、p-STAT3蛋白表达水平下降(P<0.05,P<0.01),10μg·L^(-1)IL^(-1)0组c-Myc、p-JAK2、p-STAT3蛋白表达明显增加(P<0.05,P<0.01),通路蛋白JAK2、STAT3蛋白表达未见明显改变。结论:芪苓白头翁汤可以抑制人DLBCL细胞OCI-LY10、U2932细胞的增殖并促进其凋亡,其作用机制可能与芪苓白头翁汤调控JAK2/STAT3信号通路有关。