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Abstract
Objective: To explore the effect of minimally invasive hematoma aspiration (MIHA) on the c-Jun NH2-terminal kinase (JNK) signal transduction pathway after intracerebral hemorrhage (ICH). Methods: In this experiment, 300 adult male Wistar rats were randomly and averagely divided into sham-operated group, ICH group and MIHA group. In each group, 60 rats were used in the detection of indexes in this experiment, while the other 40 rats were used to replace rats which reached the exclusion criteria (accidental death or operation failure). In ICH group and MIHA group, ICH was induced by injection of 70 µL of autologous arterial blood into rat brain, while only the rats in MIHA group were treated by MIHA 6 h after ICH. Rats in sham-operated group were injected nothing into brains, and they were not treated either, like rats in ICH group. In each group, six rats were randomly selected to observe their Bederson’s scales persistently (6, 24, 48, 72, 96, 120 h after ICH). According to the time they were sacrificed, the remaining rats in each group were divided into 3 subgroups (24, 72, 120 h). The change of brain water content (BWC) was measured by the wet weight to dry weight ratio method. The morphology of neurons in cortex was observed by the hematoxylin–eosin (HE) staining. The expressions of phospho-c-Jun NH2-terminal kinase (pJNK) and JNK in peri-hematomal brain tissue were determined by the immunohistochemistry (IHC) and Western blotting (WB). Results: At all time points, compared with the ICH groups, the expression of pJNK decreased obviously in MIHA groups (p < 0.05), while their Bederson’s scales and BWC declined, and neuron injury in the cortex was relieved. The expression level of JNK was not altered at different groups. The data obtained by IHC and WB indicated a high-level of consistency, which provided a certain dependability of the test results. Conclusion: The JNK signal transduction pathway could be activated after intracerebral hemorrhage, with the expressions of pJNK increasing. MIHA could relieve the histo-pathological damage of nerve cells, reducing brain edema and neurological deficits, and these neuroprotective effects might be associated with suppression of JNK signal transduction pathway.
Highlights
Intracereral hemorrhage (ICH), with poor prognosis, high mortality, and disability rate, is a common and frequently-occurring disease, accounting for 9%–27% in all types of stroke
There were no obvious neuromotor dysfunction on rats in the sham-operated group, while different degrees of neurological deficits were seen in ICH group and minimally invasive hematoma aspiration (MIHA) group at each time point
The results show that after treated by MIHA the Bederson’s scales of rats decrease markedly at the time points 48, 72, 96, and 120 h after ICH, compared with ICH group, which means MIHA can significantly improve the neurological deficits
Summary
Intracereral hemorrhage (ICH), with poor prognosis, high mortality, and disability rate, is a common and frequently-occurring disease, accounting for 9%–27% in all types of stroke. Though various forms of active treatment have been given in clinic, the mortality rate of ICH still remains stubbornly high owing to the absence of specific therapy [1,2,3]. Compared with traditional surgery treatment, MIHA, as a therapy aiming at removing intracranial hematoma, cannot only eliminate the space occupying effect certainly, and have advantages of less surgical trauma and better recuperation, there is no significant impact on mortality [3,4,5]. The research on the relationship between MIHA and JNK pathway has not been reported This experiment is determined to explore and investigate the influence of MIHA on the JNK signal transduction pathway and its neuroprotective effect, while the method of injecting autologous arterial blood into the rat brain is used to induce the model of ICH
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