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AIM:To establish a new rat model of depression by the antagonistic relationship of antagonizing pairs of neurotransmitters in the brain.METHODS:Dopamine D1 receptor antagonist SCH23390 was injected into the hippocampus of the rats by microinjection at low, medium and high doses (1, 2 and 4 g/L) to establish a depression model.After modeling, the sucrose consumption, open-field and novelty suppressed feeding tests were used to evaluate the behaviors of the rats, and screen out the best modeling drug dose.The model of depressive rats was induced using the best modeling drug dose and the model rats were observed for 2 weeks.The stability of the model was evaluated by behavioral tests, and the contents of IL-1β and TNF-α in cerebrospinal fluid (CSF) were measured by ELISA to evaluate the safety of the model.The levels of the antagonizing pairs of neurotransmitters in the cerebral cortex and hippocampus were analyzed by the method of high-performance liquid chromatography-mass spectrometry (HPLC-MS), so as to evaluate the pathological characteristics of neurotransmitter imbalance in the brain of the model rats.RESULTS:After modeling, the rat weight, sucrose preference rate, and horizontal motion and vertical motion scores of open-field test were significantly decreased in eACh dose model group, and feeding latent periods of novelty suppressed feeding test were significantly increased, indicating a typical depressive behavior.The rats with the medium dose (2 g/L) of SCH23390 had the most significant depressive behavior.At 2 weeks after modeling, compared with the normal control group, the weight, sucrose preference rate, and horizontal motion and vertical motion scores in medium dose group were significantly decreased (P<0.01), while the feeding inhibition time was significantly increased (P<0.05).No significant difference in the content of IL-1β and TNF-α in the CSF of normal control group, blank control group and medium dose group was observed, indicating that the model did not cause obvious inflammatory injury, and the modeling method was safe.Compared with blank control group, the contents of 5-HT, NE and Glu in the left hippocampus of rats in medium dose group were significantly increased (P<0.01), and the content of DA and ACh showed decreasing trends.The contents of 5-HT, NE and Glu in the right hippocampus of the rats were significantly increased (P<0.05), and the contents of DA and ACh showed decreasing trends.The content of Glu in cerebral cortex was significantly increased (P<0.05), the contents of 5-HT and NE showed increasing trends, and the contents of DA and ACh showed decreasing trends, indicating that the model was basically consistent with the pathological features of neurotransmitter imbalance in the brain of depression.CONCLUSION:This method can successfully replicate the rat model of depression, which has the characteristics of typical and persistent symptoms, fast modeling, and safe and easy operation.Using the dosage of 2 g/L is more suitable.
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Objective To investigate the productive effects of baicalin on the male rats with ischemic brain injury and its effects on serum progesterone level in rats; To explore the possible mechanism of baicalin in brain protection. Methods Adult SD male rats were used to create a permanent left middle cerebral artery occlusion model. The rats were evenly divided into model group, baicalin group, inhibitor group, and sham-operation group (without inserted into the intraluminal thread) according to the neurological function scores. At different time points after modeling, the neurological function scores and the grip strength of double foreleg were measured, and the reduction rate of grip strength was calculated. Serum progesterone and adrenocorticotrophic hormone (ACTH) were detected by ELISA. Results Compared with the sham-operation group, the neurological function of rats in the model group was impaired, the grip strength of double foreleg was significantly reduced. 7 days after treatment, compared with the model group, the neurological function score of baicalin group was lowered, grip strength of double foreleg was recovered, reduction rate of grip strength was reduced (P<0.05); compared with the baicalin group, protective effects of baicalin on neurological function was lowered in inhibitor group (P<0.05). 7 days after treatment, compared with the model group, the serum progesterone level in baicalin group was significantly higher (P<0.01), and ACTH level showed an increasing trend; compared with the baicalin group, serum progesterone and ACTH levels in the inhibitor group decreased (P<0.05). Conclusion The protective effects of baicalin on the male rats with ischemic brain injury may be related to the regulation of progesterone.
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Objective To investigate the effects of baicalin on serum progesterone and related hormones in female normal and cerebral ischemia rats; To explore whether baicalin plays a role in cerebral protection of neurological functions by regulating progesterone levels.Methods With vaginal smear method, the adult estrus female SD rats were selected and divided into normal group, baicalin normal group, and molding groups. The left side of the middle cerebral artery of rats in the molding groups was blocked to establish the permanent middle cerebral artery occlusion (pMCAO). After modeling, the rats were randomly divided into model group, baicalin treatment group, progesterone treatment group and progesterone inhibitor group. The baicalin normal group and baicalin treatment group were given intraperitoneal injection of baicalin solution; the normal group and model group were given normal saline of the same quantity; progesterone treatment group was given intramuscular injection of progesterone; progesterone inhibitor group was given intraperitoneal injection of baicalin solution and intragastric administration of mifepristone solution.The neurological function deficit scores were evaluated and rat forelimb holding power was detected by Grip Strength Meter respectively at different time points. Serum was taken from the rats and the progesterone and related hormones levels in the serum of every group were measured by ELISA. Results Compared with normal group, neurological functions of rats in molding groups were damaged, and neural functional behavior scores of different time points were the most strongly increased (P0.05) and more significant improvement of the forelimb holding power (P0.05).Conclusion After applying mifepristone to block progesterone, baicalin neurologic protection is significantly inhibited. The results demonstrated that baicalin may play a role in cerebral protection via up-regulating serum progesterone level.