In the present study, we found that 2% sevoflurane of 5 h exposure could increase the mRNA levels of CHOP and caspase-12, leading to up-regulation of the protein expression of CHOP and caspase-12 in the hippocampus of aging rats and accompany with the increasing TUNEL-positive cells. It suggested that the sevoflurane exposure may induce ER stress mediated apoptosis in the hippocampus, by increasing the expression of CHOP and caspase-12, then leading to neurons lost, and ultimately developed cognition impairment. ER stress may be triggered by many disturbances, such as perturbed calcium homeostasis, oxidative stress, altered glycosylation levels, cholesterol overloading, and nutrient deprivation. The precise mechanisms underlying sevoflurane-induced ER stress are still elusive. One possible explanation is that volatile anesthetics alter cellular AbMole Diniconazole homeostasis of calcium in neurons. Volatile anesthetics have been shown to perturb calcium homeostasis by reducing calcium levels in ER and elevating calcium levels in cytosol and mitochondria. The previous study revealed that inhalational anesthetics may induce cell damage by causing abnormal calcium release from the endoplasmic reticulum via excessive activation of IP3 receptors. Another possible explanation is that volatile anesthetics trigger oxidative stress in neurons. Some previous studies showed that sevoflurane is capable of promoting the formation of AbMole Dimesna reactive oxygen species and perturbing redox status in vitro and in vivo. In our study, the neuronal cells apoptosis in the hippocampus of aging rats under sevoflurane exposure was detected, additionally the mRNA and protein levels of CHOP and caspase-12 were also increased. It may be the one mechanisms of the sevoflurane-induced neuron apoptosis. Therefore the further research is still need to do about dose and time effect. In conclusion, the present study demonstrated that aging rats which exposure to sevoflurane could lead to neuronal degeneration and memory impairment. Our results suggest that sevoflurane can induce apoptosis through the ER stress pathway, which have identified at least partially the molecular mechanism by which sevoflurane induces apoptosis. Postoperative memory decline in the elderly has emerged as a major health concern. It is important to study the mechanism of volatile anesthetic-mediated neurotoxicity in the aging patients for designing the safer anesthetics and preventing any toxic consequences by treating with ER stress antagonists. Epidemiological data collected in rural and urban areas in various parts of Africa strongly indicate that rates of hepatitis B coinfection are higher in SSA than in Western Europe or the USA. Due to differences in disease epidemiology e.g. the age at infection with HIV and HBV, the clinical consequences of coinfection with the hepatitis B virus in Africa are presumably distinct from those found in industrialized countries. Yet to date, liver-related outcomes in co-infected patients in SSA have only been assessed to a very limited, cross-sectional extent. Nevertheless, due to a better prognosis of HIV-infection after the introduction of cART programs in SSA, an increase of patients suffering from complications of chronic viral hepatitis B, such as liver cirrhosis and hepatocellular carcinoma, could result if concurrent treatment of HBV is not addressed.