Samira Sahraeian, Hana Rajabpour, Mohammad Amin Edalatmanesh,
Volume 10, Issue 2 (5-2021)
Abstract
Introduction and aim: Histone deacetylase inhibitors (HDACi) have neuroprotective effects on amelioration of cerebral ischemic injuries. This study was investigated the effects of sodium butyrate (SB) as a HDACi hippocampal cell damage and neuronal/dark neuronal density in a rat cerebral hypoxic ischemia (HI) model.
Materials and Methods: In this experimental study, 40 male Wistar rats (weight: 210±10 gr) were randomly divided into 4 groups; control, HI+NS, HI+SB150 and HI+SB300. To induce The HI model after complete occlusion of the left carotid artery, animals were placed in a hypoxic chamber (containing 7.6% oxygen) for one hour. Twenty-four hours after surgery, SB was injected intraperitoneally for one week at doses of 150 and 300 mg / kg body weight. Then, the hippocampus was histopathologically studied. Cell density and neuronal dark density in the CA1, CA2, CA3 and dentate gyrus subareas were assessed by stereological method.
Results: Cell damage with increased dark neurons was observed in the different subareas of hippocampus in HI+NS group compared with the control group (p˂0.05). However, treatment with SB dose-dependently reduced cell damage and increased neuronal density in all four different hippocampal subareas (p˂0.05).
Conclusion: SB with its neuroprotective effects suppresses hippocampal neuron damage and production of apoptotic neurons in the cerebral HI model.
