LncRNA-Fendrr protects against the ubiquitination and degradation of NLRC4 protein through HERC2 to regulate the pyroptosis of microglia.

Objectives: Targeted inhibition of inflammatory response can reduce diabetic cerebral ischemia-reperfusion (I/R) injure. Pyroptosis is characterized by caspase-1 dependence and the release of a large number of pro-inflammatory factors. LncRNA-Fendrr is associated with a variety of diseases, but Fendrr has not been studied in diabetic cerebral I/R.

[Progress on perioperative monitoring of cerebral blood flow autoregulation].

Cerebral blood flow autoregulation is physiologically protective mechanism to maintain the stability of cerebral blood flow. Once autoregulation is impaired, the cerebral blood flow fluctuates with blood pressure, leading to the risk of brain ischemia or cerebral hyperemia. Multiple research results indicate that cerebral blood flow can be monitored indirectly and continuously with transcranial Doppler, near infrared spectroscopy or ICP.

Probenecid protects against transient focal cerebral ischemic injury by inhibiting HMGB1 release and attenuating AQP4 expression in mice.

Stroke results in inflammation, brain edema, and neuronal death. However, effective neuroprotectants are not available. Recent studies have shown that high mobility group box-1 (HMGB1), a proinflammatory cytokine, contributes to ischemic brain injury.

Ammonia induces upregulation of aquaporin-4 in neocortical astrocytes of rats through the p38 mitogen-activated protein kinase pathway.

Background: Astrocyte swelling is an important consequence of hepatic encephalopathy, and aquaporin-4 has been reported to play a vital role in this swelling. Ammonia causes astrocyte swelling and is also known to modulate aquaporin-4 expression in the astrocyte foot processes. The purpose of this study was to explore the mechanism of ammonia-induced aquaporin-4 expression, which has been suggested to involve the p38 mitogen-activated protein kinase pathway.

Propofol inhibits aquaporin 4 expression through a protein kinase C-dependent pathway in an astrocyte model of cerebral ischemia/reoxygenation.

Background: Aquaporin 4 (AQP4) plays a key role in maintaining water balance in the central nervous system, and its dysfunction may lead to brain edema. Previous studies have suggested that propofol may be involved in neuroprotection by preventing brain edema. In this study, we examined the effects of propofol on edema and assessed its neuroprotective actions in an oxygen and glucose deprivation (OGD) model of cultured rat astrocytes.

[Tramadol inhibits c-fos expression in spinal cord dorsal horn and serum IL-6 levels induced by plantar incision in rats].

Objective: To investigate effect of tramadol on c-fos expression in spinal cord dorsal horn and serum IL-6 levels induced by plantar incision in rats.

Methods: The Brennan pain model was induced by incision on the planter surface of left hind paw in rats. Forty-eight rats were randomly divided into six groups: Sham group (Group C), control group (Group I,pretreatment with saline 5 ml), three tramadol pretreatment groups (Group T1, T10 and T20,pretreated with 1 mg/kg, 10 mg/kg and 20 mg/kg tramadol, respectively) and one tramadol treatment group (Group PT10, treated with tramadol 10 mg/kg immediately after operation).

Propofol pretreatment attenuates aquaporin-4 over-expression and alleviates cerebral edema after transient focal brain ischemia reperfusion in rats.

Background: Cerebral edema is a major threat for stroke victims. Most studies have focused on the neuroprotective activities of propofol, addressing infarct volume rather than cerebral edema. Aquaporin-4 (AQP4) plays an important role in maintaining brain water homeostasis under various neurological insults.