Font Size: a A A

Chsgs Liver Qi Stagnation Rat Model Of Regional Cerebral Glucose Metabolism And Dopamine Type 2 Receptor Intervention Mechanism Micropet / Ct Studies

Posted on:2013-01-18Degree:DoctorType:Dissertation
Country:ChinaCandidate:L J HeFull Text:PDF
GTID:1114330371474402Subject:Chinese medical science
Abstract/Summary:PDF Full Text Request
Objective:To investigate the effect of CHSGS on regional cerebral glucose metabolism and D2R binding potential of the rat model of liver-qi stagnation syndrome by MicroPET/CT,and to study the effect of CHSGS on liver-qi stagnation syndrome through the way of neuroendocrine hormone,immunization and monoamine neurotransmitter.The study can reveal the central mechanisms of CHSGS on liver-qi stagnation syndrome and provides theoretical basis and objective visual basis.Methods:1 Establishment and evaluation of the rat model of liver-qi stagnation syndrome:We equally divided 30 rats into the normal group,model group and treatment group by adopting the open field test.The rat model was established by chronic restraint stress and isolated breeding for 3 weeks.The three groups were observed through their animal ethology,macroscopic manifestation,the level of plasma ACT,CORT,IL-6 and TNF-a,and the content of monoamine neurotransmitter in the prefrontal cortex,the hippocampus and the hypothalamus.2 The intervention mechanism study of CHSGS acting on the rat model of liver-qi stagnation syndrome through regional cerebral glucose metabolism by MicroPET/CT:60 rats were divided equally into 6 groups by adopting the open field test:normal group,model group,regeneration group,SJZT group,CHSGS low-dose group and CHSGS high-dose group.The normal group was intervented by intragastric administration of normal saline once a day for 3 weeks.The model group was intervented by chronic restraint stress and isolated breeding,and intragastric administration of normal saline once a day for 3 weeks.The regeneration group was intervented by chronic restraint stress and isolated breeding and intragastric administration of normal saline once a day for 3 weeks,then isolated breeding for one week.The SJZT group was intervented by chronic restraint stress and isolated breeding,and intragastric administration of SJZT (0.36g/mL) once a day for 3 weeks.The CHSGS low-dose group and high-dose group were intervented by chronic restraint stress and isolated breeding,and intragastric administration of CHSGS (0.52g/mL, or 1.04g/mL) once a day for 3 weeks. We observed regional cerebral glucose metabolism of each group by 18F-FDG MicroPET/CT.3 The initial intervention mechanism study of CHSGS acting on the rat model of liver-qi stagnation syndrome through regional cerebral D2R binding potential by MicroPET/CT:15 rats were divided equally into the normal group,model group and treatment group by adopting the open field test.We observed regional cerebral D2R binding potential of each group by "C-Raclopride MicroPET/CT.Results:1 Results of Experiment 1:(1)Compared with the normal group,the weight of the model group increased slowly (P<0.05),the weight of the treatment group gradually increased (P<0.05).(2) After 3 weeks, compared with the normal group,sucrose preference of the model group decreased significantly (P<0.01); in the treatment group it was higer than the former.(3) Compared with the normal group,the horizontal score and vertical score of the model group decreased significantly,the amount of stool increased (p<0.01), the immobility time of middle rele had a tendency of increasement;the horizontal score and vertical score of the treatment group were higer than that in the model group,the amount of stool decreased(P<0.05, P<0.05, P<0.01),the immobility time of middle rele had a tendency of reduction. (4)Compared with the normal group,the amount of plasma ACTH,CORT of the model group were higer than that of the former (P<0.05); there was no significant difference between the treatment group and the normal group(p>0.05),however, there was significant difference between the treatment group and the model group (P<0.05).(5)Compared with the normal group,the amount of plasma IL-6,TNF-αof the model group were lower than that of the former (P<0.05); there was no significant difference between the treatment group and the normal group(p>0.05),however, there was significant difference between the treatment group and the model group (P<0.05).(6)Compared with the normal group.the amount of 5-HT,5-HIAA and DA in the prefrontal cortex of the model group had a tendency of decreasement,the amount of NE had a tendency of increasement.However,there was no significant difference among the normal group,the model group and the treatment group(p>0.05).(7)Compared with the normal group,the amount of 5-HT,5-HIAA and DA of the model group deceased significantly (P<0.05, P<0.01, P<0.01),the amount of NE had a tendency of increasement(p>0.05); compared with the model group,the amount of 5-HT,5-HIAA and DA of the treament group inceased significantly (P<0.05, P<0.01, P<0.01),the amount of NE had a tendency of decreasement(p>0.05).(8)Compared with the normal group,the amount of 5-HT,5-HIAA and DA in the hypothalamus of the model group deceased significantly(P<.05),the amount of NE had a tendency of increasement(p>0.05);there was no significant difference between the treatment group and the normal group(p>0.05).Compared with the model group,the amount of 5-HT,DA of the treatment group increased significantly (P<0.05),the amount of 5-HIAA had a tendency of increasement,the amount of NE had a tendency of decreasement(p>0.05).2 Results of Experiment 2:(1)Compared with the normal group,there were some ROIs with increased regional cerebral glucose metabolism in the model group,such as the medulla oblongata,the left medulla oblongata, the left cerebellum and the right medulla oblongata (P<0.05); there were some ROIs with decreased regional cerebral glucose metabolism in the model group,such as the left striatum,the right prefrontal cortex,the right S1,the right S2 (P<0.01),the auditory cortex,the corpus callosum,the cingulate cortex,the M1,the M2,the S1,the S2,the insular cortex,the left corpus callosum,the left M1,the left M2,the right hypothalamus,the right hippocampus,the right corpus callosum,the right cingulate cortex,the right M1,the right M2 and the right insular cortex (P<0.05)。(2)Compared with the model group,there were some ROIs with increased regional cerebral glucose metabolism in the CHSGS low-dose group,such as the hippocampus,the FCx,the M2,the left striatum,the right auditory cortex,the right hippocampus,the right FCx,the striatum,the mesencephalon,the inferior colliculus,the auditory cortex, the corpus callosum,the Ml,the left inferior colliculus,the left hippocampus,the left corpus callosum,the left FCx,the left M2,the right striatum,the right hypothalamus,the right corpus callosum,the right Ml,the right S1,the right S2 and the right insular cortex (P<0.05);there were some ROIs with decreased regional cerebral glucose metabolism in the CHSGS low-dose group,such as the left medulla oblongata,the left visual cortex and the left cerebellum (P<0.05). (3)Compared with the model group,there were some ROIs with increased regional cerebral glucose metabolism in the CHSGS high-dose group,such as the mesencephalon and the right FCx (P<0.05).(4)Compared with the model group,there were some ROIs with increased regional cerebral glucose metabolism in the CHSGS low-dose group,such as the inferior colliculus and the left inferior colliculus (P<0.05);there were some ROIs with decreased regional cerebral glucose metabolism in the CHSGS low-dose group,such as the S2 and the right visual cortex (P<0.05).(5)Compared with the normal group,there were some ROIs with increased regional cerebral glucose metabolism in the CHSGS high-dose group,such as the medulla oblongata and the right medulla oblongata (P<0.05);there were some ROIs with decreased regional cerebral glucose metabolism in the CHSGS high-dose group,such as the S1,the S2 and the left S1 (P<0.05)3 Results of Experiment 3:(1)Compared with the normal group,there were some ROIs with increased regional cerebral D2R binding potential in the model group,such as the inferior colliculus and the left inferior colliculus(P<0.05, P<0.01),and the ROI with decresed regional cerebral D2R binding potential in the model group was striatum (P<0.05). (2)Compared with the model group.the ROI with increased regional cerebral D2R binding potential in the treatment group was striatum (P<0.05),and there were some ROIs with decresed regional cerebral D2R binding potential in the treatment group,such as the inferior colliculus.the left mesencephalon,the left pons and the left inferior colliculus (P<0.05).(3)There was no significant difference between the normal group and the treatment group.Conclusion:1 This study focuses on the animal ethology,neuroendocrine hormone,immunization, monoamine neurotransmitter.regional cerebral glucose metabolism and regional cerebral D2R binding potential.The rat model of liver-qi stagnation syndrome can be successfully established by chronic restraint stress and isolated breeding for 3 weeks.2 CHSGS has the power of treating stagnation of liver-qi syndrome,which is probably related to the level of plasma ACTH,CORT,IL-6 and TNF-a,and the content of brain 5-HT. 5-HIAA,NE and DA.3 In general, the related ROIs with regional cerebral glucose metabolic disorder of the model rat show metabolic reduction dominated by the right hemisphere.CHSGS can decrease the ROIs with increased regional cerebral glucose metabolism,and vise versa.The bidirectional modulation effect of CHSGS on regional cerebral glucose metabolism of the model rat probably is one of its central mechanism. We also get the objective visual basis.4 The ROIs with increased regional cerebral D2R binding potential in the model group are the inferior colliculus and the left inferior colliculus (P<0.05, P<0.01),and the ROI with decresed regional cerebral D2R binding potential in the model group is striatum (P<0.05).CHSGS can rectify the disorder of regional cerebral D2R binding potential of the model group.The bidirectional modulation effect of CHSGS on regional cerebral D2R binding potential of the model rat probably is one of its central mechanism. We also get the objective visual basis.5 Compared with the normal group and the model group,the change trends of regional cerebral glucose metabolism of the CHSGS low-dose group or high-dose group basically is the same with each other,with different change ranges.In general,the curative effect of the CHSGS low-dose group is superior to the CHSGS high-dose group,which points out that the dose-effect relationship is complicated.6 The MicroPET/CT is a powerful tool in research of syndromes and Chinese herbs,which can provide objective visual basis and integrate clinical and basic research findings.
Keywords/Search Tags:CHSGS, liver-qi stagnation syndrome, MicroPET/CT, 18F-FDG, 11C-Raclopride
PDF Full Text Request
Related items