Objective To investigate the expression of Polo-like kinase 1 in renal clear cell carcinoma and tissue adjacent to carcinoma;impact of BI2536 on the cell proliferation of renal clear cell carcinoma A498 cell line.Methods We select 12 cases of renal cancer Specimens of randical surgery between January 2013 and December 2014.The study included 7 male patients and 5 female patients,whose age ranged from 41 to 68 years(mean 49 years).Tumors were single and the location of tumor included 5 in left kidney,7 in right kidney.The size of renal tumor ranged from 2.1 to 6.3 cm.All patients did not have radiotherapy and chemotherapy preoperative who have no local and distant matastasis.The pathological results demonstrated renal clear cell carcinoma in 12 cases.At the same time,we collect the tissue 2 centimeters away as control,which pathological results demonstrated normal tissue.The expression of PLK1 was detected by western bloting in tissues from 12 cases of renal clear cell carcinoma and tissue adjacent to carcinoma and quantitative analysis was made.Cell proliferation of A498 cell line at the different concentrations of BI2536 were assayed by flow cytometry (0,20,40,60μg/L).Results The expression of PLK1 in renal clear cell carcinoma tissue are 0.74 ±0.2 and 0.21 ±0.13.The carcinoma tissue is higher than tissue adjacent to carcinoma (P =0.02).BI2536 act on A498 after 48 hours,the A498 cell number were arrested at G2/M phase at 0μg/L,20μg/L,40μg/L and 60μg/L were (10.28 ± 0.47) ％,(14.35 ± 0.85) ％,(20.49 ± 0.78) ％ and (23.90 ± 0.54) ％,respectively.The A498 cell number were arrested at G2/M phase increase when we incearse the concentrations of BI2536 at 48 hours (P ＜ 0.05).Conclusions The higher expression of PLK1 in renal clear cell carcinoma and the proliferation of the renal clear carcinoma cell can be repressed by BI2536 both reveal PLK1 may be used as the molecular maker and therapeutics target of renal clear cell carcinoma.

OBJECTIVE To establish a met hod for the determination of amentoflavone ，bilobetin，ginkgetin，isoginkgetin and sciadopitysin in Ginkgo biloba leaves tablets. METHODS After extracted with methanol ，ultra-performance liquid chromatography （UPLC）was adopted to determine G. biloba leaves tablets. The determination was performed on Waters Acquity UPLC HSS T 3 column with acetonitrile- 0.4％ phosphoric acid as mobile phase （gradient elution ）at the flow rate of 0.4 mL/min. The column temperature was set at 35 ℃，and the detection wavelength was 340 nm. The sample size were 1 μL（substance control ）and 10 μL （test sample ）. The relative correction factors （RCFs）of bilobetin ，ginkgetin，isoginkgetin and sciadopitysin were calculated by quantitative analysis of multicomponents by single marker （QAMS）using amentoflavone as control. The chromatographic peak was located with the relative retention time method. Then the contents of the above components were calculated ，and the results were compared with those of external standard method （ESM）（except for amentoflavone ）. RESULTS The linear ranges of amentoflavone，bilobetin，ginkgetin，isoginkgetin and sciadopitysin were 0.10-8.21，0.24-19.34，0.16-12.98，0.22-17.66，0.06-4.86 ng，respectively（all r＞0.999）. The quantitation limits were 0.10，0.24，0.16，0.22，0.06 ng，respectively. RSDs of precision ， repeatability and stability tests （36 h）were all lower than 3.00％. The average recoveries were 99.77％-102.85％，and RSDs were 1.90％-4.40％（n＝6）. The average RCFs of bilobetin ，ginkgetin，isoginkgetin and sciadopitysin were 0.91，0.93，0.96 and 0.95， respectively. The average relative retention times were 1.08，1.18，1.19 and 1.30，respectively. The relative deviation between the calculation result of QAMS and ESM was within ±3.00％. CONCLUSIONS The established method is accurate and stable ，and can be applied to the determination of Ginkgo biflavones in G. biloba leaves tablets and control the quality.

Atherosclerosis is a chronic vascular inflammatory disease caused by abnormal lipid metabolism.The formation of lipid-rich foam cells acts as the initial trigger for development of atherosclerotic lesions.Recent studies have shown that lipophagy,a form of selective autophagy,can selectively degrade lipid droplets stored intracellularly and promote cholesterol efflux through the autophagic lysosomal pathway.As a result,intracellular lipid accumulation is re-duced and foaming is inhibited,making lipophagy a potential new target for current anti-atherosclerosis therapy.This arti-cle reviews the crucial role and molecular mechanism of lipophagy in the link between lipid metabolism and atherosclero-sis.Its objective is to outline the regulatory mechanism of lipophagy and present fresh insights for the treatment of athero-sclerotic diseases.