| Intracerebral hemomhage (ICH) is defined as the rupture of blood vessels within the brain parenchymal. It is a common clinical emergency that has high incidence, high mortality. Especially in critically ill patients, the mortality rate is about 30%-50% within 30 d, the prognosis is poor. The Chinese medicine treatment has good effects on the ICH in clinic, but the lack of scientific proof, and the mechanism of little, thus the research and application of Chinese medicine is difficult to combine with the world. So to in-depth study the mechanism of Chinese medicine on the ICH has great significance.The previous results showed that the baicalin enhanced the SOD activity, reduced the MDA and NO levels and inhibited the NOS activity to reduce the free radical damage and nerve toxicity. In addition, the baicalin also increased the inhibitory amino acids (IAA) levels and decreased the excitatory amino acids (EAA) levels to protect the damaged brain tissue with the ICH.The GABA plays physiological activity through recognizing and combining with three specific GABA receptors(GABARs):GABAAR, GABABR and GABAcR. The GABAAR is the most abundant and important recepter among GABARs in the mammalian brains. GABA transporter (GAT) can quickly uptake the GABA in the synaptic cleft and extracellular fluid to terminate the effect of GABA on the postsynaptic membrane receptors and end the process of GABA in the synaptic transmission. Studies found that some neurodegenerative diseases such as amyotrophic lateral sclerosis, Alzheimer's disease and Parkinson's psychosis, as well as some nervous system damage such as trauma, ischemia and ICH had the apoptosis involved by Caspase-3. The antiapoptotic protein Bcl-2 plays an important role in neural development and neurological diseases.Methods and objective:The intracerebral hemorrhage rat model was induced by collagenase+heparin sodium. The rats were randomly divided into sham group, model group and treatment group. Rats of sham group and model group were treated with physiological saline, the treatment group were treated with baicalin at the dosage of 200 mg/kg. The morphological changes of neurons were detected by the HE staining method; the positive cells of GAT-1, GABAAR, Caspase-3 and Bcl-2 were detected by the immunohistochemistry staining method; and the apoptosis rates were detected by the flow cytometry (FCM). The research was aimed to explore the protection mechanisms of baicalin on brain injury after ICH in rats and to provide theoretical basis for further understanding the pathogenesis of ICH and developing ICH protective agents.Results:1. Induction of ICH and observation of nerve morphology:The results showed that the significant changes of behaviors and neurons in rats with ICH. After administrating with baicalin, the rats significantly improved on behaviors and returned to normal at the 3rd day. At the same time, the cerebral hemorrhage conditions had been released and the damaged neuronal cells had been improved significantly.2. The expression of GAT-1 and GABAAR:The results of immunohistochemical staining showed that compared with the sham group, the expression of GAT-1 was up-regulated in 12 h after ICH,24 h expressed the highest,72 h still expressed a certain intensity,7 d after the return to normal levels; The expression of GABAAR was up-regulated in 12 h after ICH,24 h began to decrease,72 h down to the lowest,7 d to return to normal levels. Compared with the model group, the number of GAT-1 positive neurons was obviously decreased and the number of GABAAR positive neurons was obviously increased in the treatment group. The average optical density was positive correlation with the number of positive neurons.3. Detection of apoptosis:The results of immunohistochemical staining showed that the Caspase-3 positive neurons were increased at 1st day after ICH, increased greatly at 3rd day and began to decline at 7th day. The expressions of Bcl-2 at 1st day after ICH were found, a peak at 3rd day, began to decline at 7th day. After administrating baicalin, the Caspase-3 positive neurons were decreased greatly, the Bcl-2 positive neurons were increased. The apoptosis rate of model group was higher than that of treatment groups.Conclusion:These results show that the GAT-1 and GABAAR may be involved in the pathophysiological process of neuronal injury after ICH in rats. The apoptosis is an important mechanism of brain injury after ICH. Baicalin decreased GAT-1 expression and increased the GABAAR expression, as well as inhibit the Caspase-3 activation and increase Bcl-2 expression in brain after ICH to reduce and inhibit the neuron apoptosis, and promote the survival of neurons, and thus protect the brain from injury.
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