ABSTRACT
Objective:To study the relationship among lipoprotein‐associated phospholipase A2 (Lp‐PLA2 ) gene A379V and T403V locus polymorphisms and genetic susceptibility of coronary heart disease (CHD) .Methods:Lp‐PLA2 gene A379V and T403V locus polymorphisms of 160 coronary angiography confirmed CHD patients (CHD group ) and 117 healthy subjects (healthy control group ) were measured using gene sequencing technique .ELISA was used to measure blood lipids and plasma Lp‐PLA2 level in two groups ,and they were compared between two groups . Results:Compared with healthy control group ,there were significant rise in age ,male proportion ,plasma levels of hs‐cTnI ,hsCRP ,TC ,LDL‐C , Lp (a) ,WBC ,mononuclear cells (MNCs) and Lp‐PLA2 [ (119.98 ± 49.41) ng/ml vs .(248.59 ± 76.51) ng/ml] ,and significant reduction in HDL‐C level in CHD group ( P<0.01 all) .The CC , CT , TT genotype and C , T allele were de‐tected all in A379V and T403C locus of two groups .Compared with healthy control group ,there were significant rise in frequencies of CC genotype (1.7% vs .9.3% ) and C allele (13.7% vs .20.3% ) of Lp‐PLA2 gene T403C locus in CHD group , P< 0.05 both . All genotypes and alleles of A379V locus possessed no significant difference between CHD and healthy control group . Conclusion:Plasma Lp‐PLA2 level may be related to CHD risk .Lp‐PLA2 gene T403C locus poly‐morphism possesses certain relationship with genetic susceptibility of CHD .
ABSTRACT
Objective To observe the effect of autophagy on paclitaxel-induced CaSki cell death through the regulation of the expression of autophagy gene Beclin1, and to explore the interaction and relationship between autophagy and apoptosis. Methods Eukaryotic expression vector pcDNA3.1-Beclin1 and RNA interference vector pSUPER-Beclin1 were transfected into human cervical cancer CaSki cells in vitro and screened for stable expression cell lines. The formation of autophagic vacuoles was observed with an electronic microscope. The expression of Beclin1 and LC3 was measured by Western blot. After being treated with paclitaxel, the change of cell proliferation was assessed by MTT assay, the percentage of apoptotic cells and autophagic cells were analyzed by flow cytometry. Results A lot of autophagic vacuoles were observed in pcDNA3.1-Beclin1 cells by electronic microscopy. Beclin1 and LC3 protein expression was up-regulated in CaSki cells transfected with pcDNA3.1-Beclin1, and was inhibited in cells transfected with pSUPER-Beclin1. MTT assay revealed the survival rate of CaSki cells was significantly decreased after being transfected with pcDNA3.1-Beclin1. After being treated with paclitaxel, the percentages of apoptotic cells and autophagic cells were both increased in pcDNA3.1-Beclin1 group compared with that of the blank control group especially the increase of apoptosis was particularly evident. Conclusion Autophagy and apoptosis have different roles in the process of paclitaxel-induced cervical cancer CaSki cell line death. Overexpression of Beclin1 in CaSki cells may enhance the apoptosis induced by paclitaxel.