Glutamate-mediated oxidative stress causes neuronal cell death by increasing intracellular Ca2+ uptake, reactive oxidative species (ROS) generation, mitogen-activated protein kinase (MAPK) activation, and translocation of apoptosis-inducing factor (AIF) to the nucleus. In the current study, we demonstrated that corydaline exerts potent neuroprotective effects against glutamate-induced neurotoxicity. Treatment with 5 mmol/L glutamate increased cellular Ca2+ influx, ROS generation, MAPK activation, and AIF translocation. In contrast, corydaline treatment decreased cellular Ca2+ influx and ROS generation. Western blot analysis revealed that glutamate-mediated MAPK activation was attenuated by corydaline treatment. We further demonstrated that corydaline treatment inhibited the glutamate-mediated translocation of AIF to the nucleus. We propose that corydaline is a promising lead structure for the development of safe and effective neuroprotectants.

Alcohol intake is known to affect various organs in the human body, causing reduction of salivation in the oral cavity. Hypo-salivation effect of alcohol is a common feature, but the mechanism in salivary glands is still poorly studied. Therefore, in this study, the changes in salivary secretion and water channel protein (aquaporin5, AQP5) in salivary glands of mice were investigated after ethanol administration. Animals were divided in to 4 groups with the control, 4 g/kg ethanol, 8 g/kg ethanol and 16 g/kg ethanol administration groups. One hour after ethanol administration, saliva was collected from the oral cavity, and the animals were killed and parotid and submandibular glands were extracted to analyze the histopathology, AQP5 immunihistochemistry and AQP5 protein level. According to the results, the salivation rate decreased irrespective of the ethanol dose in mice, and viscosities increased with increase in ethanol dose. However, there were no pathological changes in parotid and submandibular glands due to ethanol administration. Expression of AQP5 in parotid and submandibular glands decreased with increase ethanol administration These results indicate that the reduction of salivary secretion due to acute alcohol intake is closely related to decrease of the water channel protein such as AQP5 in parotid glands and submandibular glands, rather than the damage of salivary glands.

Type1 diabetes mellitus (DM) is generally known to be caused by destruction of insulin-producing pancreatic β cells or an immune-related problem. Polydipsia is a representative symptom of DM, and it has been reported that this condition is closely related to xerostomia and is considered that hyposalivation from the salivary gland results in this phenomenon. Although various studies have reported that induction of diabetes reduces endogenous stem cells in other organs (heart, brain etc.), diabetes-related changes in endogenous stem cells in the salivary gland have not yet been well established. Therefore, in this study, to verify the change in salivary gland stem cells after diabetes, salivary gland tissues in the control and diabetes-induced groups were processed by histochemistry (Masson’s trichrome staining) for morphological analysis, TUNEL assay for cell death, and immunohistochemistry (Ki-67 and c-Kit) for cell proliferation and maturation. Diabetes induced by STZ leads to vacuolization, apoptosis, and reduction in proliferating cells/salivary gland stem cells in salivary glands of rats. This result suggests that diabetes may be associated with reduction in salivary gland function such as degeneration and inhibition of regeneration in the salivary gland.