ABSTRACT In recent years, many studies have unraveled the impact of microRNAs (miRNAs) in intracerebral hemorrhage (ICH). This study aims to explore the role of miR-93 in modulating neurological function,… Click to show full abstract
ABSTRACT In recent years, many studies have unraveled the impact of microRNAs (miRNAs) in intracerebral hemorrhage (ICH). This study aims to explore the role of miR-93 in modulating neurological function, cerebral edema and neuronal apoptosis of rats with ICH by regulating TLR4/NF-κB signaling pathway. ICH models were constructed using Ⅶ collagenase method. The successfully modeled rats were injected with miR-93 antagomir, TLR4/NF-κB signaling pathway activator or inhibitor together with their controls. The expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β) and vascular endothelial growth factor (VEGF) was measured using enzyme-linked immunosorbent assay (ELISA). The expression of human aquaporin 4 (AQP-4), Caspase-3, Bax, Bcl-2 and TLR4/NF-κB signaling pathway-related proteins was also measured. MiR-93, TLR4 and NF-κB were all highly expressed in ICH, reduced miR-93 and inhibited TLR4/NF-κB signaling pathway could improve neurological function and suppress inflammation in ICH rats. Moreover, down-regulated miR-93 and suppressed TLR4/NF-κB signaling pathway were able to attenuate cerebral edema and abate pathological lesion. We have also found in this research that miR-93 knockdown as well as inhibited TLR4/NF-κB signaling pathway could relieve neuronal apoptosis in ICH rats. This study suggests that reduced miR-93 alleviates the neurological function and cerebral edema as well as repressed neuronal apoptosis of ICH rats via the inhibited activation of TLR4/NF-κB signaling pathway.
               
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