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AIM:To investigate the role of specific binding of precursor form of nerve growth factor(proNGF) to p75NTR(proNGF-p75NTR)in isoflurane-induced cognitive impairment in aging mice.METHODS: Aging C57BL/6J male mice were randomly divided into 3 groups:control group,isoflurane(Iso)group and p75NTR specific inhibitor 2-ami-no-3-methyl-pentanoic acid amide(LM11A-31,LM)+isoflurane(LM+Iso)group.Aging C57BL/6J mice in Iso group and LM+Iso group were exposed to isoflurane,and the mice in control group were exposed to air.The mice in LM+Iso group were treated with LM,which dissolved in normal saline water and was administered daily by oral gavage at 50 mg· kg-1· d-1for 1 month.The mice in control group and Iso group received an equivalent volume of normal saline by the same route.Arterial blood gas analysis was conducted to detect the physiological state of the mice after isoflurane exposure. Morris water maze was performed to evaluate the cognitive function.The protein levels of proNGF,p75NTR,phosphorylated p38 MAPK and cleaved caspase-3 were determined by Western blot.RESULTS: Compared with the control group, the protein expression of proNGF and p75NTR in the hippocampus of Iso group was significantly elevated(P<0.05).The phos-phorylation level of p38 MAPK was higher in Iso group than that in control group(P<0.05),which was reduced in LM +Iso group significantly(P<0.05).A significant increase in the protein level of cleaved caspase-3 was observed in Iso group as compared with control group(P<0.05), while LM11A-31 treatment reversed this elevation significantly(P<0.05).The escape latency prolonged and the number of crossing the original platform location reduced in Iso group com -pared with control group(P<0.05), which were reversed by LM11A-31 in LM+Iso group(P<0.05).CONCLU-SION:ProNGF-p75NTR probably plays an vital role in the apoptotic pathway activation and the cognitive dysfunction in ag -ing mice exposure to isoflurane,which provides a potential target for clinical intervention.
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Objective To observe the effect of Natural mountain spring on oxidative damage of aging mice . Methods Thirty male aging mice were randomly divided into experimental group ( drink Natural mountain spring ) and control group ( drink tap water ) according to the level of MDA .The serum in the two groups was taken for T-SOD activity and MDA content analysis after two months .Results The MDA content in experimental group decreased markedly than that in control group .Conclusion Natural mountain spring could alleviate oxidative damage by free radicals to extent .
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@# ObjectiveTo observe the imitation of menopause and the change of spatial cognition in mice administrated with D-galactose and to evaluate the molecular mechanism of estrogen to protect the function of hippocampal neurons.MethodsAdult female C57BL/6 mice were bilateral ovariectomy (OVX) and subcutaneously treated with D-galactose (100 mg/kg). In estrogen replacement therapy(ERT) mice were i.p. administrated with E2 (50 μg/kg). It took 8 weeks to induce the model and treat with ERT. Morris water maze was used test the function of spatial learning and memory. Estrogen and oxidative stress enzymes were detected by kit. 8-oxo-dG was immunohistochemical stained, and the expression of MTH1 in brain hippocampus was detected by Western blotting.ResultsThe level of E2 in blood in model group was one fifth of that in Sham group(P<0-01), and E2 level obviously increased in ERT group; the escape latency significantly prolonged in model group(P<0-01), and obviously shortened in ERT group(P<0-05). SOD and GSH-Px significantly reduced and MDA obviously increased in model group(P<0-05); and approached normal in ERT group. 8-oxo-dG as a DNA oxidative damage marker was obviously increased in the hippocampus of model group. However, the expression of DNA repair protein MTH1 significantly reduced(P<0-05), and both of them returned to normal in ERT group(P<0-05).ConclusionEstrogen can improve the function of spatial cognition in aging mice model by repairing the DNA damage of hippocampal neurons.
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Object To study the effects of gypenosides on MAO and Na/K ATPase activities in brain tissues of aging mice Methods Models of aging mice were prepared by continuous post orbitol injection of 120 mg/kg D galactose for a month, then the effects of gypenosides on MAO and Na/K ATPase activities in brain tissues were investigated Results It was observed that MAO activity was increased and Na/K ATPase activity was decreased in brain tissues of aging mice models significantly; and these effects were reversible respectively by gypenosides ig of 75 and 150 mg/kg Conclusion The result that gypenosides could invert the changes of MAO and Na/K ATPase activities in brain tissues of aging mice, may provide a further explaination of the anti aging mechanism of gypenosides in molecule enzymology