Neuroprotective effect of sulfated pachymaran on the MPTP-induced Parkinson mice / 中国药理学通报

Aim To determine the neuroprotective effect of sulfated pachymaran (SP)on MPTP-induced mouse model.Method ICR mice were randomly di-vided into control group,MPTP group and SP treatment group (50,1 00,1 50 mg·kg -1 ,ip).After 1 7 days, the activities of endogenous antioxidants (SOD,GSH-Px,CAT),antisuperoxide anion,hydrogen peroxide and MDA content in the midbrain and cortex were as-sayed.Results The results proved that SP significant-ly reduced the content of MDA and H2 O2 ,regulated the activities of antioxidant enzyme and increased the activity of antisuperoxide anion.Conclusion All these effects indicate that SP is a potential neuroprotective a-gent and its neuroprotective effects are achieved in the MPTP mouse model.

Hippocampal neuron damage and cognitive dysfunction of diabetic Wistar rats / 生物医学工程学杂志

This study aimed to explore the cognitive dysfunction of and hippocampal neuron damage to Wistar rats with STZ-induced diabetes at different morbidity time. All Wistar rats in the tests received intraperitoneal injections of streptozotocin (STZ; 60 mg/kg) to induce type 1 diabetes. The concentration of blood glucose and the body weight were investigated, the cognitive ability of rats was assessed using a standardized Y-maze, and the apoptotic neurons in the CA1 of the hippocampus were also examined by using the HE staining. While the sickening time was prolonged, the blood glucose concentration of the experimental rats increased continuously and the body weight decreased. On the 70th day after STZ administration, the neuronal loss in the hippocampal CA1 region increased and the working errors increased in rats with the diabetes. The results showed that Wistar rats could complicate with diabetic encephalopathy in 70 days after injection of STZ for inducing the diabetes.

Advances of researches on caspases in neurodegenerative diseases / 生物医学工程学杂志

Acute and chronic neurodegenerative diseases are illnesses associated with high morbidity and mortality, and few or no effective options are available for their treatments. Many neurodegenerative diseases are included in them, for example, stroke, brain trauma, spinal cord injury, amyotrophic lateral sclerosis (ALS), Huntington's disease, Alzheimer's disease, and Parkinson's disease. Given that central nervous system tissue has very limited, if any, regenerative capacity, it is of utmost importance to limit the damage caused by neuronal death. During the past decade, considerable progress has been made in understanding the process of cell death. In this article, we review the causes and mechanisms of neuronal-cell death, especially as it pertains to the caspases family of proteases associated with cell death. The results may be helpful to the experimental research and clinical application of neurodegenerative diseases.