Abstract
The present study was aimed to investigate the effects of minocycline (MC) on the expression of nerve growth factor (NGF) and heat shock protein 70 (HSP70) following intracerebral hemorrhage (ICH) in rats, and explore the neuroprotective function of MC. Seventy-eight male SD rats were randomly assigned to three groups: the ICH control group ( n = 36), ICH intervention group ( n = 36) and sham operation group ( n = 6). The ICH control group and ICH intervention group were subdivided into 6 subgroups at 1, 2, 4, 5, 7 and 14 d after ICH with 6 rats in each subgroup. Type IV collagenase was injected into the basal nuclei to establish the ICH model. All rats showed symptoms of the nervous system after the model was established, and the sympotsm in the ICH control group were more serious than the ICH intervention group. The number of NGF-positive cells and HSP70-positive cells in the ICH intervention group was higher than that of the ICH control group. MC administration by intraperito-neal injection can increase the expression of NGF and HSP70. MC may inhibit the activation of microglia, the inflammatory reaction and factors, matrix metalloproteinases and apoptosis, thus protecting neurons. The change of the expression of NGF and HSP70 may be involved in the pathway of neuroprotection by MC.
Highlights
Intracerebral hemorrhage (ICH) is typically caused by spontaneous rupture of blood vessels
Brain edema begins within hours, and can last for weeks, which contribute to neurological deterioration by increasing intracranial pressure, even causing a shift in brain structures[2]
We used type IV collagenase injected into the caudate nucleus stereotaxically to establish the intracerebral hemorrhage (ICH) model that reflects the clinical pathological process
Summary
Intracerebral hemorrhage (ICH) is typically caused by spontaneous rupture of blood vessels. It is an important public health problem with a high incidence and high mortality and exerts a heavy economic and social burden worldwide. During ICH, blood rapidly enters the brain parenchyma, which may further disrupt the blood brain barrier (BBB), impair delivery of oxygen and glucose to cells and result in secondary bleeding. Brain edema begins within hours, and can last for weeks, which contribute to neurological deterioration by increasing intracranial pressure, even causing a shift in brain structures[2]. The primary injury after ICH is physical destruction that compresses the surrounding structures and increases intracranial pressure. The secondary injury is neurological deterioration including hematoma expansion, edema, inflammation and neuron death in the brain parenchyma surrounding the hematoma[3]
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