Résumé
Objective To investigate the changes of the level of oxidative stress and cell apoptosis of secondary brain injury after traumatic brain injury,and the influence of brain-derived neutrophic factor on these parameters in rats,as well as its potential mechanisms.Methods A total 84 adult and healthy male rats was divided randomly into 2 groups:control (n =42) and traumatic brain injury (TBI) groups (n =42).The brain-derived neurotrophic factor (BDNF) group was induced using improved Feeney method and was received abdominal injections of BDNF (0.5 μg/μl) immediately after injury,the control group were received abdominal injections with the same dose sodium chloride injection immediately after injury and repeat one time everyday until the rats was killed.Each group was divided into seven subgroups by sacrificed time after injury,those are 1 h,3 h,6 h,12 h,24 h,3 d,and7 d,each subgroup got6 rats.Each subgroup was randomly selected three rats after being killed.The water content,superoxide dismutase (SOD),malonic aldehyde (MDA),and glutathione (GSH) of rats were measured contusion peri tissues brain tissue.Specimens were taken from left three rats of subgroup,which was part of the brain tissue.The expression of NF-κB p65,around the brain tissue with immunohistochemical methods were detected.TdT-mediated dUTP nick-end labeling (TUNEL) method was used to observe the peri cell apoptosis after brain contusion.Results NF-κB p65 was expressed obviously around the lesion in 1h group,and strongly expressed in TBI-3 h-12 h,and reached a peak in 24 h after the injury,while NF-κB p65 expression reduced in TBI-3 d-7 d,and still in high expression.NF-κB p65 expression strongly correlated with the degree of cerebral edema (r =0.651,P ＜0.05).For two groups,NF-κB p65 expression strongly correlated with the level of MDA (r1 =0.947,P ＜0.01;r2 =0.961,P ＜0.01).Conclusions Changes of NF-κB protein expression after brain injury were involved in a series of pathological processes of secondary brain injury,such as oxidative stress,and apoptosis,brain-derived neutrophic factor is probably through inhibit oxidative stress levels,control apoptosis,prevent the development of vasogenic cerebral edema,and reduce or mitigate secondary brain injury.
Résumé
Objective To explore the effect of schisanhenol on adipokine expression in 3T3-L1 adipocyte and its related mechanism. Methods 3T3-L1 adipocyte was cultured in vitro and induced to differentiation and maturity. Glucokinase was added to culture medium to make an oxidative model. The expression of adipocytokines were detected under the circumstance of different doses and at different time points of schisanhenol. Results The expression of adiponectin, leptin, resistin and visfatin were decreased with the increase of glucokinase concentration. Concentration-dependent inhibition effect was most obvious in leptin (25 mU/ml Glucokinase vs Blank group, t =7.29, P＜0.01). With pretreatment of oxidative stress, the adipocytokines increased as the doses of schisanhenol increased (t=6.31,P＜0.01 in adiponectin;t=5.92, P＜0.01 in leptin; t=3.77, P＜0.05 in resistin; t=3.63,P＜0.05 in visfatin). With the extension of schisanhenol effect, the expression of four adipokines showed the process of first decrease-then increase'. The effects of schisanhenol on adipokines were parallel with the alteration of oxidative stress. Conclusions Schisanhenol increased adipocytokines expression in 3T3-L1 adipocyte by reducing oxidative stress, and the increase of leptin and adiponectin were most obvious, which indicated that schisanhenol could play a role in the treatment of diabetes by Chinese herb wuweizi.