1.STUDY OF GALLIC ACID IN PU-ERH TEA ON THE PEROXISOME PROLIFERATORS ACTIVATED RECEPTORS FUNCTION
Dongying ZHANG ; Wanfang SHAO ; Zhonghua LIU ; Yalin LIU ; Yewei HUANG
Acta Nutrimenta Sinica 1956;0(01):-
Objective To study the effect of gallic acid isolated from Pu-erh Tea on the peroxisome proliferators activated receptors function.Method The appropriate concentration of gallic acid added to three cell models was decided to be 50 ?g/ ml,and the activity of gallic acid on peroxime prolipevators activated receptors PPAR?,PPAR?,PPAR? was studied.Results Gallic acid could activate PPAR?,as high as 2.436 fold and the effect corresponded to that of positive drug which value was 2.438.gallic acid had no effect on PPAR? and PPAR?.Conclusion Gallic acid in Pu-erh Tea had good activity on PPAR? and this could offer scientific basis for study of the anti-diabetes and anti-hyperlipidenmia mechanism of Pu-erh Tea.
2.Clinical effect of Zhanjinhuoxue Formula combined tower-type pad natural traction for treating pure thoracolumbar compression fracture
Yewei LIU ; Yuxiang ZHANG ; Xiaosong HUANG ; Xiangnan SHEN
Chongqing Medicine 2017;46(9):1246-1248
Objective To investigate the clinical effect of Zhanjinhuoxue Formula combined with the tower-type pad natural traction for the treatment of pure thoracolumbar compression fracture.Methods Fifty patients with thoracolumbar compression fractures treated in our hospital from January to December 2014 were selected and divided into the observation group(n=25) and control group(n=25).The control group was given the tower-type natural traction method,while the observation group was given Zhanjinhuoxue Formula combined with the tower-type pad natural traction method.The curative effect,pain score,activity ability score,analgesic drugs score,bone mineral density (BMD) and the Japanese Orthopedic Association(JOA) score were compared between the two groups.Results The effective rate was 92.00% in the observation group and 68.00% in the control group,the difference between the two groups was statistically significant (x2 =4.50,P<0.05).The pain score,activity ability score and analgesic drugs score after 6-month treatment in the observation group were significantly lower than those in the control group (P<0.05);the BMD and JOA scores in the observation group were significantly higher than those in the control group (P<0.05).Condusion Zhanjinhuoxue Formula coordinated by the tower-type pad natural traction method can conduce to alleviate the pain symptom in the patients with pure thoracolumbar compression fracture,increases the movement function and improves the treatment effect.
3.Inhibition of SIRT6 in prostate cancer reduces cell viability and increases sensitivity to chemotherapeutics.
Yewei LIU ; Qian Reuben XIE ; Boshi WANG ; Jiaxiang SHAO ; Tingting ZHANG ; Tengyuan LIU ; Gang HUANG ; Weiliang XIA
Protein & Cell 2013;4(9):702-710
SIRT6 is an important histone modifying protein that regulates DNA repair, telomere maintenance, energy metabolism, and target gene expression. Recently SIRT6 has been identified as a tumor suppressor and is down-regulated in certain cancer types, but not in other cancers. From deposited gene profiling studies we found that SIRT6 was overexpressed in prostate tumors, compared with normal or paratumor prostate tissues. Tissue micro-array studies confirmed the higher levels of SIRT6 in both prostate tumor tissues and prostate cancer cells than in their normal counterparts. Knockdown of SIRT6 in human prostate cancer cells led to sub-G1 phase arrest of cell cycle, increased apoptosis, elevated DNA damage level and decrease in BCL2 gene expression. Moreover, SIRT6-deficiency reduced cell viability and enhanced chemotherapeutics sensitivity. Taken together, this study provides the first evidence of SIRT6 overexpression in human prostate cancer, and SIRT6 regulation could be exploited for prostate cancer therapy.
Apoptosis
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Cell Cycle Checkpoints
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Cell Line, Tumor
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Cell Proliferation
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Cell Survival
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DNA Damage
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Drug Resistance, Neoplasm
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Gene Knockdown Techniques
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Humans
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Male
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Prostatic Neoplasms
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genetics
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pathology
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therapy
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Proto-Oncogene Proteins c-bcl-2
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metabolism
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Sirtuins
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antagonists & inhibitors
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genetics
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metabolism
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Up-Regulation