Introduction: Hyperammonemia has an important role in neuroinflammation induced by cirrhotic hepatic encephalopathy (HE). Mitogen-activated protein (MAP) kinases have shown to play key roles in the signaling pathways from inflammatory receptors. Nowadays mesoporous silica such as SBA-15 has received considerable attention as a drug delivery vehicle because of its large surface area and pore volume for loading drugs and large biomolecules. It has been shown that nanoporous silica type SBA-15 have a possible potential to control increased levels of ammonia in HE. In this study, we aimed to evaluate the possible therapeutic effects of subcutaneous injection of SBA-15 in a rat model of HE. Methods: We used male Wistar rats weighing 300-350 g and cirrhotic chronic liver failure was induced with a common bile duct ligation (BDL) in a group of rats as a model of HE. Sham control operation consisted of laparotomy and bile duct identification without ligation and resection. SBA-15 (0.2 mg/kg) was injected subcutaneously with 48 hours intervals during 28 days of BDL. On day 28 of BDL, each rat was decapitated, rat brain removed, and the prefrontal cortex (PFC) and the hippocampus were dissected. Total RNA extraction and cDNA synthesis were performed and real-time qPCR method was used to evaluate gene expression of jnk3 MAP kinase. Results: The present results revealed that in the hippocampus and PFC of the HE model rats, p38 Map kinase gene expression was increased while the jnk3 gene expression was significantly decreased. The results also showed that SBA-15 treatment during 28 days induction of cirrhotic liver failure and HE, returned the change in the gene expression of p38 MAP kinase to a normal level. Conclusion: It is concluded that SBA-15 nanopores may have an effect on increased level of ammonia in the brain of rat model of HE. One may propose that SBA-15 nanopores can have a therapeutic potential in controlling HE.
