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Effects of Acori Graminei Rhizoma Extract on GABA Transporter 1 and Glutamate Transporter 1 Expression in Developing Rat Hippocampus after Recurrent Seizures

Author: HuangZuo
Tutor: MaoDingAn
School: Central South University
Course: Pediatrics
Keywords: Convulsions Developmental stages γ- aminobutyric acid transporter 1 Glutamate transporter 1 Shichangpu extract
CLC: R285.5
Type: Master's thesis
Year: 2011
Downloads: 43
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Abstract


Objective: To study the development of rat hippocampus after recurrent seizures γ-aminobutyric acid transporter (γ-aminobutyric acid transport 1, GAT1) and glutamate transporter 1 (glutamate transport 1, GLT1) expression changes and Shichangpu extract (acori graminei rhizome extract, AGR) and the effects of ten pre explore GAT1 and GLT1 seizures in early childhood brain injury in the pathogenesis of the role and Shichangpu extract the possible mechanism of anticonvulsant. Methods: after birth (postnatal, PN) 7-day total of 72 SD rats were randomly divided into three groups: control group, seizure group, Shichangpu extract ten pre-group, n = 24 rats in each group was randomly divided into three parts, respectively, in the last convulsions after (after recurrent seizures, ARS) 1d, 3d, 7d (equivalent to PN-13d, 15d, 19d) brains were removed. By trifluoromethyl ether repeated inhalation (6 consecutive days, day 1) seizures developing rats produced an animal model. Were used immunohistochemistry and Western blot detection of recurrent seizures in rats in each group after 1d, 3d, 7d hippocampus GAT1 and GLT1 protein. Results: (a) Immunohistochemistry results showed that: ① In the control group GAT 1PN-13d, PN-15d and PN-19d, the control group GAT1 immunohistochemistry average optical density (average optical density, AOD) value without significant difference; PN-13d (ARS-1d), PN-15d (ARS-3d) and PN-19d (ARS-7d), the seizure rats hippocampus immunohistochemistry AOD GAT1 expression was significantly higher than the control group ( P lt; 0.01); Shichangpu ten pre-set GAT1 immunohistochemistry AOD group was significantly lower than the convulsion (P lt; 0.01), compared with the control group had no significant difference; ② GLT1 in the control group at each time point immunohistochemical AOD values No significant differences; PN-13d (ARS-1d), and PN-19d (ARS-7d) when the seizure group GLT1 immunohistochemistry AOD values ??than the control group was significantly higher (P lt; 0.01), while the PN-15d (ARS -3d) when compared with the control group had no significant difference: PN-13d, PN-15d and PN-19d when Shichangpu extract ten pre-set GLT1 immunohistochemistry AOD values ??and control groups compared with seizures were significantly higher (P lt; 0.01) (two) Western blot results showed that: ① In the control group, PN-19d when compared with PN-13d and PN-15d when GAT1 protein expression was significantly decreased (P lt; 0.05); seizure rats ARS-1 d ( PN-13d), ARS-3d (PN-15d) and ARS-7d (PN-19d) when, GAT1 protein expression was significantly higher in the intervention group and shichangpu (P lt; 0.01); in ARS-3d (PN -15d) and ARS7d (PN19d), the intervention group than in the control group Shichangpu Roundup was significantly higher (P lt; 0.01), while the ARS-1d (PN-13d) Shichangpu intervention group than in the control group had no significant difference Roundup ( P gt; 0.05). ② In the control group, PN-13d, PN-15d and PN-19d hippocampal GLT1 protein Roundup no significant difference; seizure group ARS-1d (PN-13d), ARS-3d (PN15d) and ARS-7d ( PN-19d) hippocampal GLT1 protein expression was significantly increased compared with the control group (P lt; 0.01); ARS-1d (PN-13d), ARS-3d (PN-15d) and ARS-7d (PN-19d), the Shichangpu extract intervention group than in the seizure group and the control group were significantly increased. Conclusions: (1) neonatal recurrent seizures in hippocampus area may cause abnormal expression of GAT1 and GLT1, the imbalance of expression may be involved in both developmental brain damage seizures pathological process; (2) adjust the freshman big Shichangpu extract recurrent seizures caused by rat brain hippocampus area GAT1 and GLT1 expression imbalance.

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