Abstract
BackgroundAs we known, Traditional Chinese Medicine (TCM) helps to prevent the relapse of drug addiction. However, the scientific basis of TCM remains unclear because of limitations of current reductionist approaches. We aimed to explore the possible mechanism of how ANKK1 TaqIA (A1/A2) [rs1800497(T/C)] affects the relapse of opioid addiction on the perspective of Chinese traditional medicine.MethodsThe ANKK1 TaqIA (A1/A2) [rs1800497(T/C)] of the dopamine D2 receptor (DRD2) polymorphisms were genotyped in a case–control sample consisting of 347 opioid addicts and 155 healthy controls with RT-PCR and the TCM pathological factors were collected by means of Syndrome Elements Differentiation in the case–control sample.ResultsDRD2/ANKK1 TaqIA Polymorphisms has no relation with opioid addiction relapse; but for those who were diagnosed with phlegm syndrome, DRD2/ANKK1 TaqIA Polymorphisms affect the replapse of apioid addiction (P < 0.05).ConclusionsDRD2/ANKK1 TaqIA is associated with opioid addict and it is obvious in opioid addicts who suffer from the phlegm syndrome.
Highlights
As we known, Traditional Chinese Medicine (TCM) helps to prevent the relapse of drug addiction
Studies on animal models further underline the role of Dopamine D2 Receptor (DRD2) in drug addiction as the rewarding effects of opiates were found absent in mice lacking the D2 receptor gene [3, 4]
Later it turned out that the TaqIA restriction fragment length polymorphism (RFLP) is located approximately 10 kilobases downstream from the DRD2 gene, in exon 8 of the Ankyrin repeat and kinase domain containing 1 (ANKK1) gene [9], which is a member of the serine/threonine kinase family
Summary
Traditional Chinese Medicine (TCM) helps to prevent the relapse of drug addiction. We aimed to explore the possible mechanism of how ANKK1 TaqIA (A1/A2) [rs1800497(T/C)] affects the relapse of opioid addiction on the perspective of Chinese traditional medicine. A kind of chronic brain disease relapses, which is caused by abuse of heroin, morphine, interacts with the reward system of brain [1]. An interesting hypothesis has arisen from the possible roles of decreased dopamine receptor density resulting in Reward Deficiency Syndrome [2]. Studies on animal models further underline the role of DRD2 in drug addiction as the rewarding effects of opiates were found absent in mice lacking the D2 receptor gene [3, 4]. The protein product of the ANKK1 gene was considered as a negative regulator of the NF-κB (Nuclear Factor-KappaB)
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