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1.
Article in Chinese | WPRIM | ID: wpr-1021861

ABSTRACT

BACKGROUND:Inhibitory control and drug craving are the core elements of evaluating drug withdrawal in methamphetamine addicts,which has attracted much attention in academic circles.As we all know,in order to achieve complete abstinence from drug addiction,the key is to restore the damaged inhibition and control function of drug addicts and effectively reduce the craving for drugs. OBJECTIVE:To systematically analyze the relationship between exercise and methamphetamine abstinence inhibitory control and drug craving,to find out an effective exercise intervention scheme that can promote methamphetamine abstinence,and to further explore the internal mechanism of exercise,in order to provide theoretical support and applied reference for the future use of exercise in drug withdrawal. METHODS:CNKI,WanFang,VIP,Web of Science,and PubMed databases were searched for relevant literature using the keywords of"exercise,physical activity,methamphetamine,inhibitory function,craving,addiction"in Chinese and"sport*,exercise,methamphetamine,drug craving,executive function,addiction"in English.According to the inclusion and exclusion criteria,86 documents were finally included for review. RESULTS AND CONCLUSION:In terms of inhibitory control in methamphetamine abstinent individuals,either acute and long-term moderate-intensity aerobic exercise or acute high-intensity interval training can significantly improve the inhibitory control capacity of methamphetamine abstinent individuals.For long-term aerobic exercise,aerobic group exercise or full-body comprehensive exercise is more effective.If the exercise format is power cycling,it is recommended to increase the frequency of exercise intervention.In terms of the drug craving intensity in methamphetamine abstinent individuals,acute moderate-intensity aerobic exercise and resistance training,as well as long-term moderate-intensity,high-intensity,or progressive load aerobic and resistance training,can effectively reduce the drug craving in methamphetamine abstinent individuals.Exercise exerts intrinsic regulatory effects on methamphetamine-mediated addiction.Exercise can influence the expression of tyrosine hydroxylase in the brain's ventral tegmental area,thereby stimulating the expression of dopamine receptor coupling proteins and promoting dopamine synthesis in the brain's reward regions,thereby compensating for dopamine depletion caused by methamphetamine addiction.Furthermore,exercise can also regulate protein kinase A inhibitors,affecting the protein kinase A signaling pathway mediated by dopamine D1 receptors,by inhibiting protein kinase A,thus affecting cAMP response element-binding protein and regulating methamphetamine addiction.Additionally,exercise can also,at the genetic level,affect the expression of the c-fos gene in the brain's nucleus accumbens region,activate a subset of glutamatergic neurons in this area,generate a rewarding effect,and thus improve methamphetamine addiction.Although current research has confirmed the relationship between exercise and methamphetamine addiction and has clarified the brain mechanisms underlying the effects of exercise,whether there are other brain regulatory pathways for the effects of exercise remains to be explored through more scientifically rigorous animal or human experiments,starting from the cellular or molecular level.

2.
Yao Xue Xue Bao ; (12): 1240-5, 2015.
Article in Chinese | WPRIM | ID: wpr-505040

ABSTRACT

This study was conducted to investigate the paclitaxel loaded by hydrazone bonds in poly(ethylene glycol)-poly(caprolactone) micelles (mPEG-PCL-PTX) on proliferation and apoptosis of human lung cancer A549 cells and its possible mechanisms of anti-tumor activity. The cell proliferation was measured with MTT assay. Flow cytometry were used to analyze the cell cycle. The cell apoptosis was analyzed using Hoechst/P staining. The expression levels of apoptotic genes expression in the mitochondrial apoptosis pathway were detected by RT-PCR and Western blotting, respectively. The mPEG-PCL-PTX could inhibit the proliferation of A549 cells and promote the apoptosis. The Bax, caspase-3 protein expression were increased while Bcl-2 protein expression was decreased in A549 cells. Results showed that the polymer containing hydrazone bond is non-toxic in vitro, the mPEG-PCL-PTX micelles can inhibit the proliferation and induce the apoptosis of A549 cells. Key words: paclitaxel; micelle; A549 cell; proliferation; cell cycle; apoptosis

3.
Article in Chinese | WPRIM | ID: wpr-480371

ABSTRACT

Aim: To determine the uptake characteristics of salvianolic acid B(Sal B) in myocardial cells and blood vessel endothelial cells. Method: The effects of various factors, such as time, temperature, drug concentration, pH of the medium, on the uptake of Sal B in myocardial cells and aorta endothelial cells were investigated. LC/MS was employed to determine the intracellular concentration of Sal B. Results: Uptake kinetics of Sal B in the myocardial cells and aorta endothelial cells fitted well to the logarithmic model at 37 ℃ and 4 ℃. The a-mount of uptake was in direct proportion to the extracellular concentration of Sal B in the experimental concentration range. Uptake of Sal B both in the myocardial cells and blood vessel endothelial cells would significantly increase while the medium pH decreased, and some water-soluble components extracted from danshen would also facilitate the uptake of Sal B both in the myocardial cells and blood vessel endothelial cells obviously. The energy metabolism inhibitors would significantly inhibit the uptake of Sal B in the myocardial cells and blood vessel endothelial cells. When lactic acid and fatty acid were added to the incubation solution, the uptake of Sal B both in the myocardial cells and aorta endothelial cells increased more than 20%. Conclusion: pH is the most important factor influencing the cellular uptake of Sal B, and the amount of uptake tends to increase in acidic medium. Results suggest that the uptake of Sal B would increase in the acidified internal environment induced by myocardial ischemia, thus exerting better cardiovascular activities.

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