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ObjectiveTo investigate the effects of pentoxifylline (PTX) on oxidative stress in brains of epileptic (EP) rats based on the nuclear factor E2 related factor 2 (Nrf2) antioxidant response element (ARE) signal pathway.MethodsThirty-six healthy and adult male Wistar rats were included in the experiment and were divided into blank control group (peritoneal injection of isotonic saline), EP control group (induced EP episode), and PTX group (induced EP episode ＋ PTX pretreatment) according to a completely random method, then 12 rats in each group. The behavioral changes of rats in each group were monitored, and the EP attack rate and seizure latency were recorded. The rats were sacrificed to collect substantia nigra and hippocampus for testing oxidative stress indicators and expression levels of Nrf2 ARE signaling pathway-related proteins.ResultsNo abnormal reaction was observed in the control group after treatment. The EP attack rate in the EP control group reached 83.33%. The EP attack rate (33.3%) and the attack level ((2.14±0.40) vs (3.09±0.58)) in the PTX group were significantly lower than those in the EP control group, and the seizure latency was significantly longer than that in the EP control group (P0.05) ). The expression of substantia nigra tissue was significantly higher than that of the blank control group (P<0.05).ConclusionPTX can inhibit EP seizure and improve the oxidative stress in the brain of rats at the early stage of EP. The possible mechanism is that PTX can specifically activate Nrf2 ARE signaling pathway.
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Objective To study the effect oftenuigenin (TEN) on the processes of neural stem cells (NSCs) injured by β-amyloid (Aβ) protein. Methods Mouse NSCs were generated from the hippocampi of Kunming mice within 24 hour from birth and cultured with epidermal growth factor (EGF)and basic fibroblast growth factor (bFGF) (20 ng/mL each) in 50-mm uncoated culture flasks.The third passage NSCs were cultured in Aβ medium (12.5 μmol/L) and TEN medium (5 mg/L,20 mg/L,100mg/L) respectively and observed under a scanning electron microscope (SEM) after 3 days.Optical microscopy was used to detect the length and amount of the processes of NSCs. The statistical significance between group comparisons was determined by t test.P value ＜0.05 was considered to be statistically significant. Results The length and amount of NSC processes in Aβ1-42 group were both significantly shorter and smaller than in the control group (P＜0.05). The length and amount of NSC processes in 20 mg/L and 100 mg/L groups were both significantly longer and larger than in the Aβ-42group (P＜0.05). Conclusion TEN can significantly increase the length and amount of NSC processes injured by Aβ.
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Objective To determine the effect of Tenuigenin (TEN) on the Mashl expression in neural stem cells (NSCs) from mouse hippocampus and directional differentiation of its NSCs in vitro. Methods NSCs were generated from the mouse hippocampus within 24 hours after birth and cultured with EGF and bFGF (20 ng/mL, each) in a 50-mm uncoated culture flask. The third-passage NSCs were cultured with TEN medium and divided them into vehicle, 5 mg/L, 20 mg/L and 100 mg/L groups according to different TEN concentrations. Immunocytochemical techniques were employed to detect the NSE-positive neurons and ChAT-positive neurons induced by TEN, and the expression of Mash1 in NSCs affected by TEN was measured by RT-PCR techniques. Results The immunocytochemical and RT-PCR results revealed that ChAT-positive neurons and NSE-positive neurons were detected with statistical significance and 20 mg/L group showed a stronger effect than other concentration groups (P< 0.05). The expression of Mash1 in the 20 mg/L group increased as compared with that in the vehicle group (P<0.05). Conclusion TEN can induce NSCs in vitro differentiating into neurons and cholinergic neurons, and increase the expression of Mashl in NSCs.