Abstract
Early brain injury (EBI) has been considered as the major contributor to the neurological dysfunction and poor clinical outcomes of subarachnoid hemorrhage (SAH). Studies showed that apelin-13 exhibits a neuroprotective effect in brain damage induced by cerebral ischemia. However, it remains unclear whether apelin-13 could exhibit the protective functions following SAH. The present study aimed to validate the neuroprotective role of apelin-13 in SAH, and further investigated the underlying mechanisms. We constructed SAH rat model and we found that apelin-13 significantly alleviated neurological disorder and brain edema, improved memory deficits in SAH rats. Apelin-13 treatment decreased contents of TNF-α and IL-1β in cerebral spinal fluid of SAH rat by using ELISA. Apelin-13 treatment promoted the expression of APJ and Bcl-2, and decreased the level of active caspase-3 and Bax in the temporal cortex after SAH by using western blot. Also, apelin-13 attenuated the cortical cell death and neuronal degeneration as shown by TUNEL, FJB and Nissl staining. However, ML221, an inhibitor of APJ, significantly reversed all the above neuroprotective effects of apelin-13. Moreover, a neuron-microglia co-culture system, which mimic SAH in vitro, confirmed the protective effect of apelin-13 on neurons and the inhibitory effect on inflammation through apoptosis-related proteins. These data demonstrated that apelin-13 exhibit a neuroprotective role after SAH through inhibition of apoptosis in an APJ dependent manner.
Highlights
Subarachnoid hemorrhage (SAH) is reported to be related with elevated rates of mortality and morbidity, which accounts for about 5% of all stroke cases [1]
A neuronmicroglia co-culture system, which mimic subarachnoid hemorrhage (SAH) in vitro, confirmed the protective effect of apelin-13 on neurons and the inhibitory effect on inflammation through apoptosis-related proteins. These data demonstrated that apelin-13 exhibit a neuroprotective role after SAH through inhibition of apoptosis in an APJ dependent manner
We evaluated the effects of apelin-13 on neurological impairment, brain edema, neuroinflammation and spatial memory deficits in a rat SAH model
Summary
Subarachnoid hemorrhage (SAH) is reported to be related with elevated rates of mortality and morbidity, which accounts for about 5% of all stroke cases [1]. EBI has been regarded as the major contributor to the neurological dysfunction and poor clinical outcomes in patients following SAH [4, 5]. Therapeutic inhibition of EBI may represent a novel and promising approach in the management of SAH cases. Elucidating the underlying molecular mechanism of EBI is critical for develop novel and effective therapeutic approach against SAH. Brain injury (EBI) has been considered as the major contributor to the neurological dysfunction and poor clinical outcomes of subarachnoid hemorrhage (SAH). Studies showed that apelin exhibits a neuroprotective effect in brain damage induced by cerebral ischemia. It remains unclear whether apelin-13 could exhibit the protective functions following SAH. The present study aimed to validate the neuroprotective role of apelin-13 in SAH, and further investigated the underlying mechanisms
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