Articles: subarachnoid-hemorrhage.
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Neuroinflammation is an early event of brain injury after subarachnoid hemorrhage (SAH). Whether the macrophage mediators in resolving inflammation 1 (MaR1) is involved in SAH pathogenesis is unknown. In this study, 205 male Sprague-Dawley rats were subjected to SAH via endovascular perforation in the experimental and control groups. ⋯ Jumonji d3 (JMJD3) protein levels tended to increase and peaked at 24 h after SAH. LGR6 and JMJD3 expression were co-localized with microglia. (ii) MaR1 administration mitigated short-term neurological deficits, brain edema and long-term neurobehavioral performance after SAH, and attenuated microglial activation and neutrophil infiltration. (iii) Knockdown of LGR6, inhibition of CREB phosphorylation or JMJD3 activity abolished the anti-neuroinflammatory effect of MaR1 on the expression of CREB, CBP, JMJD3, IRF4, IRF5, IL-1β, IL-6 and IL-10, thus prevented microglial activation and neutrophil infiltration. Together, the results show that MaR1 can activate LGR6 and affect CREB/JMJD3/IRF4 signaling to attenuate neuroinflammation after SAH, pointing to a potential pharmacological utility in this disorder.
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The triglyceride glucose (TyG) index is regarded as a reliable alternative indicator for measuring insulin resistance. We investigated the association between the prognosis of patients with subarachnoid hemorrhage (SAH)and the TyG index, explored the potential of the TyG index as a new biomarker for forecasting the outcomes of SAH patients, and explored independent risk factors for predicting the condition of SAH patients. ⋯ Patients with SAH may benefit from using the TyG index as a predictive method. In our clinical practice, the TyG index is beneficial for managing diseases and making decisions. More research is required to determine if improved TyG index control would lead to better clinical results in the future.