1.Effect of Ghrelin on L-type Calcium Channel Current of Ventricular Myocytes in Experimental Rats
Bo YANG ; Daoliang ZHANG ; Youzhi HU ; Jinfeng XIAO ; Chengzhi ZHOU
Chinese Circulation Journal 2014;(10):832-835
Objective: To study the effect of ghrelin on L-type calcium channel current (ICa-L) of ventricular myocytes in experimental rats. Methods: The single ventricular myocyte in experimental rats were obtained by enzymolysis method, and the whole-cell patch-clamp technique was used to investigate the effect of ghrelin on ICa-L of ventricular myocytes at different doses of 10 nmol/L, 100 nmol/L and 1μmol/L respectively. Results: Ghrelin at 10 nmol/L, 100 nmol/L and 1μmol/L may inhibit ICa-L at (8.95 ± 2.13) %, (31.18 ± 4.78) % and (64.63 ± 8.57)% respectively,P<0.05, and the current-voltage curve was shifted upwards. The channel half inactivation curve decreased from (-1.34 ± 1.9) mV to (-8.04 ± 1.32 ) mV, (9.76 ± 1.17) mV and (-11.81 ± 0.73) mV respectively,P<0.05, and the recovery time after inactivation was prolonged as τ value from (63.23 ± 9.32) to (98.95 ± 10.74), (109.56 ± 13.42) and (127.39 ± 16.13) respectively,P<0.05. Conclusion: Ghrelin may accelerate ICa-L inactivation and prolong the recovery time after inactivation. Ghrelin inhibits ICa-L in a dose-dependent manner.
2.Application of Myofascial Trigger Points Theory in Clinical Practice of Sports Rehabilitation (review)
Lin LIU ; Qiangmin HUANG ; Qingguang LIU ; Chengzhi BO
Chinese Journal of Rehabilitation Theory and Practice 2016;22(10):1167-1170
This article demonstrated the myofascial trigger points theory and the application of related techniques in the clinical prac-tice of sports rehabilitation, such as the treatment of athletes injury pain, rehabilitation of movement function limitation, elimination of sports fatigue and so on. The clinical treatments based on the myofascial trigger points theory are simple, effective, noninvasive, and with short recovery time and low recurrence rate. It provides scientific theoretical and practical foundation for the prevention, diagnosis, treat-ment and rehabilitation for sport injury.
3.Protection Effect of Wogonin on Mice with Hyperlipidemia
Bo YANG ; Chengzhi ZHOU ; Daoliang ZHANG ; Youzhi HU ; Jinfeng XIAO
Herald of Medicine 2014;(10):1310-1313
Objective To explore the effects of wogonin on hyperlipidemia in mice and clarify the molecule mechanism. Methods Thirty mice were evenly divided into three group normal control group,model control group and treatment group. The normal control group was given normal diet,the model control group received high-fat diet,the treatment group received high-fat diet with wogonin (500 mg·kg-1 ). Results The mice developed hyperlipidemia 12 weeks after starting the high-fat diet. The body weight,visceral fat and fat index were increased (P<0. 05). After treatment,these indices were reduced ( P < 0. 01). Wogonin significantly reduced the total cholesterol ( TC),low density lipoprotein ( LDL),high density lipoprotein (HDL),except the triglyceride (TG). Compared to the model control group,the hepatic lipase(HL) and lipoprotein lipase(LPL) activity in the treatment group were recovered (P<0. 05),but HMG-CoA reductase activity was inhibited ( P<0. 01). Mechanistic study suggested that the lipid-lowering effect might be related to the lipid synthesis genes (SREBP-1c,FAS, PPARγ) and the lipid metabolism genes (PPARα,CPT-1). Conclusion Wogonin can prevent hyperlipidemia,which might be related to the regulation of enzyme activity and the changes of lipid synthesis and oxidative metabolism.
4.Baicalin attenuates Aβ25-35 induced learning and memory disorders in mice and its possible mechanism
Wan XIAO ; Xiaolu CAO ; Rong ZHANG ; Chengzhi GAO ; Jing DU ; Tingzi YIN ; Ying ZHANG ; Xing HONG ; Xiamin HU ; Bo REN
Chinese Journal of Pharmacology and Toxicology 2017;31(1):59-64
OBJECTIVE To observe the effect of baicalin on Aβ25-35 induced learning and memory deficits and changes in autophagy-related genes in mice so as to explore the related mechanisms of Alzheimer disease (AD) treatment . METHODS C57 mice were administered with 3μL Aβ25-35 3 mmol·L-1 by intracerebroventricular injection to establish an AD model. Baicalin was given by intracerebroventricular injection at the dose of 25, 50 and 100 mg · kg-1 for 15 d, respectively. The total distance and the central grid residence time were measured in the open-field test. The escape latency and the time to reach the platform were monitored in the Morris water maze trial. The autophagic vacuoles in the hippocampus of the mice were observed by transmission electron microscopy before the protein expressions of microtu?bule-associated protein 1 light chain 3 (LC3) and Beclin1 in brain tissue were analyzed by Western blot?ting assay. RESULTS Intracerebroventricular injection of Aβ25-35 could reduce the total distance from (3984±321)cm to (2790±306)cm and extend central grid residence time from (3.6±1.2)s to (8.8±2.9)s in the open-field test. The escape latency of water maze also increased from (22.0 ± 1.9)s to (38.8 ± 2.2)s. Autophagic vacuoles or late autophagic vacuoles and increased Beclin1 and LC3 and protein level were observed in the hippocampus after Aβ25-35 injection. Intraperitoneal injection of Baicalin 50 and 100 mg · kg-1 for fifteen consecutive days extended the total distance in open-field test to (3705 ± 337)cm and (3968 ± 448)cm, respectively, while the central grid residence time was reduced to (5.6 ± 1.8)s and (3.9±1.5)s, respectively. The total time taken to reach the platform in water maze test was reduced to (28.6± 1.9)s, (22.9 ± 1.7)s. Mitochondrial swelling, vacuolar membrane structure or autophagic vacuoles were visible in the hippocampus. LC3 and Beclin1 protein expression was significantly up-regulated(P<0.01). CONCLUSION Baicalin shows protective effect against Aβ25-35 induced learning and memory deficits, and this effect may be related to the activation of autophagy in the mouse hippocampus.
5.Risk factors and etiology in young adults with ischemic stroke
Bo SONG ; Lei WANG ; Li GAO ; Jinmin LI ; Chengzhi DAI
International Journal of Cerebrovascular Diseases 2018;26(3):178-183
Objective To investigate the risk factors and etiology in young adults with ischemic stroke.Methods From June 2014 to June 2017,consecutive patients with first-ever ischemic stroke aged from 18 to 45 years and admitted to the Department of Neurology,the Third People's Hospital of Chengdu were collected retrospectively.The demographic data,vascular risk factors,National Institutes of Health Stroke Scale score,location of infarction,and etiological subtypes were documented.They were divided into either a male group or a female group according to the gender,and they were divided into 2 age groups of 18-35 years and 36-45 years.Results A total of 103 young adults with ischemic stroke were enrolled during the study.Among them,the proportion of men was higher than that of women (73.8% vs.26.2%).The most common 5 risk factors were smoking,abnormal lipid metabolism,drinking alcohol,hypertension,and large atherosclerosis,respectively.The proportions of abnormal glucose metabolism (37.2% vs.11.8%),hypertension (46.5% vs.11.8%),and large artery atherosclerosis (37.2% vs.11.8%) in the age group of 36-45 years were significantly higher than those in the age group of 18-35 years (all P<0.05).The proportions of smoking (67.1% vs.14.8%) and drinking alcohol (51.3% vs.18.5%) in the male group were significantly higher than those in the female group (all P< 0.05).In the etiological aspect,the proportion of cryptogenic stroke in the age group of 18-35 years was significantly higher than that in the age group of 36-45 years (47.1% vs.15.1%;P=0.006),while the proportion of the large artery atherosclerotic stroke was significantly lower than that in the age group of 36-45 years (11.8%vs.41.9%;P =0.019).There were no significant differences in the etiological subtypes between different sex groups.Conclusion The distribution of risk factors and etiological subtypes in young patients with ischemic stroke have some differences in different gender and age groups.Some common modifiable risk factors (such as smoking,drinking,abnormal lipid metabolism,etc.) still account for a higher proportion in young adults with ischemic stroke.