1.Effects of resveratrol-induced cellular autophagy in control of neurodegenerative diseases.
Acta Pharmaceutica Sinica 2016;51(1):18-22
Cellular autophagy is a major degradative pathway for clearance of aggregate-prone proteins and damaged organelles. It plays an important role in regulating cellular homeostasis, cell growth and development, and disease development. Dysfunctional autophagy contributes to the pathology of various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, in which specific pathological protein accumulation occurs. A growing body of evidence suggests that resveratrol plays a significantly role in the regulation of autophagy and clearance of pathological proteins. Resveratrol is a potential drug for neurodegenerative diseases therapy. This review focuses on the effects of resveratrol on cellular autophagy and clinical application in the control of neurodegenerative diseases.
Alzheimer Disease
;
Autophagy
;
Humans
;
Huntington Disease
;
Neurodegenerative Diseases
;
drug therapy
;
Parkinson Disease
;
Stilbenes
;
pharmacology
3.Effects of resveratrol-induced cellular autophagy in control of neurodegenerative diseases.
Acta Pharmaceutica Sinica 2016;51(1):18-22
Cellular autophagy is a major degradative pathway for clearance of aggregate-prone proteins and damaged organelles. It plays an important role in regulating cellular homeostasis, cell growth and development, and disease development. Dysfunctional autophagy contributes to the pathology of various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, in which specific pathological protein accumulation occurs. A growing body of evidence suggests that resveratrol plays a significantly role in the regulation of autophagy and clearance of pathological proteins. Resveratrol is a potential drug for neurodegenerative diseases therapy. This review focuses on the effects of resveratrol on cellular autophagy and clinical application in the control of neurodegenerative diseases.
4.Impact analysis of comorbidities on prognosis of myelodysplastic syndromes patients.
Wei YAN ; Wen-xu HU ; Rong ZHANG
Chinese Journal of Hematology 2012;33(7):574-576
Adolescent
;
Adult
;
Aged
;
Female
;
Humans
;
Male
;
Middle Aged
;
Myelodysplastic Syndromes
;
diagnosis
;
epidemiology
;
Prognosis
;
Young Adult
5.Correlation between Tetramine Poisoning and Hypocalcemia in Children
Ai-rong, HUANG ; Wen-jie, ZHENG
Journal of Applied Clinical Pediatrics 2006;0(18):-
Objective To investigate the correlation between tetramine poisoning and hypocalcemia in children.Methods According to different severe cases grade,tetramine poisoning children were divided into critical group(70-90 score),extremely critical group(
6.Study on Quality Standard of Hovenia dulcis Thunb Extract
Wei WEN ; Hong ZHANG ; Rong ZENG
Chinese Journal of Information on Traditional Chinese Medicine 2006;0(05):-
Objective To establish a quality standard of Hovenia dulics Thunb. Method The presence of quercetin was identified and assayed by TLC and HPLC, respectively. Result Linearity of marker was obtained over the range of 1.32 ~ 5.28 ?g (r =0.9999). The average recovery rate was 98.78% (RSD=1.08%). Conclusion TLC is specific. The method of quality is accurate, reappearance, simple, rapid, and suitable for the quality control of Hovenia dulcis Thunb.
7.Effect of Fangjifulingtang on Proliferation and PAI-1 in Glomerular Mesangial Cells
Rong YU ; Xiaobai ZHANG ; Xiaodong WEN
Chinese Journal of Information on Traditional Chinese Medicine 2006;0(08):-
Objective To investigate the effect of Fangjifulingtang on preventing proliferation of glomerular mesangial cells and the expression of PAI-1, so as to provide experimental evidence for Fangjifulingtang to cure chronic kidney disease. Method Glomerular mesangial cells were cultured and TNF-? was used as a stimulation to make the cells proliferate. Then Fangjifulingtang was incubated together at different doses. Cell vitality were evaluated and qualified by MTT. Cell period were analysed by Flow CytoMeter (FCM). Secretion of PAI-1 expression was measured by ELISA. Results The proliferation of Glomerular mesangial cells was inhibited (P
8.Prevalence and related factors of peptic ulcer in military personnel of China
Wen WANG ; Xiaojun WANG ; Rong WANG
Medical Journal of Chinese People's Liberation Army 2001;0(09):-
Objective To investigate the prevalence and related factors of peptic ulcer (PU) and Helicobacter pylori (Hp) infection in military men. Methods A stratified multi-stage cluster randomly sampling method was used. A questionary survey was conducted in 6 160 soldiers garrisoned at south China, inclding: PU symptoms and risk factors questionnaires; gastroscopy and Hp detection. Results Incidence of PU correlative symptoms (Sc≥5) in soldiers was 18.60%. The prevalence of PU was 12.78%.Higher incidence of PU was found among the soldiers who enlisted for less than 1 year, or were from south China, or served in armored troops. The prevalence of Hp infection was 62.67%. Hp infection (OR4.60), smoking (OR3.8), sustained intense training (OR4.3), fighting vehicle driving (OR6.0) and frequent mental intension (OR3.7) seemed to be the main risk factors of PU. While hot food, milk and whether or not the only child in a family showed no relation with PU incidence. Conclusion Higher prevalence of PU and Hp infection existed in service men. For soldiers, PU incidence is closely associated with Hp infection, military training, mental factors, and also related to soldiers′ enlisted period, arm of the service and the region where the soldiers come from.
9.Cardiomyocyte and renal cell apoptosis induced by overtraining and the preventive effects of anisodamine in rats
Guangli WU ; Junfang RONG ; Jinkun WEN
Medical Journal of Chinese People's Liberation Army 1982;0(01):-
Objective To study the cardiomyocyte and renal cell apoptosis induced by overtraining, and the preventive effects of anisodamine against the adverse effects. Methods The rats were forced to swim till exhaustion to reproduce the animal model of overtraining. The animals were randomly divided into control group, exhausted group and anisodamine group. The exhausted group, depending on the recovery time after exhaustion, was divided again into exhaustion subgroup, 6h after exhaustion subgroup, and 24h after exhaustion subgroup. The animals in the anisodamine group received intraperitoneally 10mg/kg of anisodamine before the swimming overtraining, and divided again into 6h after anisodamine injection subgroup and 24h anisodamine injection subgroup. The cardiomyocyte and renal cell apoptosis was observed by the method of TUNEL, image analysis and flow cytometry. Results It was revealed by TUNEL that the number of apoptotic cardiomyocytes was increased after exhaustive swimming, especially in the 6h after exhaustion subgroup. The number of apoptotic cells was also increased in kidney of 0h, 6h and 24h after exhaustion subgroups, especially in 24h after exhaustion subgroup. The apoptosis ratio was also increased significantly in 0h, 6h and 24h after exhaustion subgroups as demonstrated by flow cytometry. Compared with the rats of exhausted group, the number of apoptotic cells in heart and renal tissue was decreased remarkably after anisodamine injection. Conclusion The apoptosis of cardiomyocyte and renal cell could be induced by exhaustive swimming. Compared with kidney, heart injury recovered more quickly. Anisodamine had the preventive effect on the injury to heart and kidney in exhausted rats.
10.Advances in origin and pathogenesis of epithelial ovarian cancer.
Chinese Journal of Pathology 2011;40(8):569-572
Adenocarcinoma, Clear Cell
;
etiology
;
pathology
;
Brenner Tumor
;
etiology
;
pathology
;
Carcinosarcoma
;
etiology
;
pathology
;
Cell Transformation, Neoplastic
;
Cystadenocarcinoma, Serous
;
etiology
;
pathology
;
Epithelial Cells
;
metabolism
;
pathology
;
Female
;
Genes, p53
;
Humans
;
Mutation
;
Neoplasms, Glandular and Epithelial
;
etiology
;
genetics
;
metabolism
;
pathology
;
Ovarian Neoplasms
;
etiology
;
genetics
;
metabolism
;
pathology
;
Tumor Suppressor Protein p53
;
genetics
;
metabolism