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Objective: To investigate the effects of fosinppril on myocardial cell apoptosis and apoptosis-associated gene expression in chronic heart failure (CHF) rats. Methods: CHF model was established by partially banding of abdominal aorta superior to renal artery. The experimental rats were randomly divided into 3 groups: Sham operation group and CHF group, the rats in both groups received stomach normal saline; Fosinopril group, the rats received stomach fosinopril 10 mg/kg?d.n=10 in each group and all animals were treated for 8 weeks. LVEDP, ±dp/dtmax and LVMI were examined, left ventricular myocardial cell apoptotic index (AI) was measured by TUNEL method, Bcl-2 and Bax protein levels were detected by immunohistochemistry and caspase-3 protein expression was assessed by Western blotting. Results: Compared with Sham operation group, CHF group had increased LVEDP, LVMI, AI, elevated protein expressions of Bax and Caspase-3,P Conclusion: Fosinopril may inhibit myocardial cell apoptosis which occurred during CHF, by up-regulating Bcl-2 expression and down-regulating expressions of Bax and Caspase-3 in CHF rats, therefore improve the cardiac function.
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Objective To investigate the protective effect and its mechanism of DL-3-n-Butylphthalide on the brain damage in rats following whole brain irradiation.Methods A total of 120 male Sprague Dawley rats were randomly divided into sham-irradiation group,irradiatien group and DL-3-n-Butylphthalide group.The model of whole-brain irradiatien was established by exposuring rat brain to 4 MeV X-rays with a single-dose of 10 Gy.The rats were intraperitoneally injected with DL-3-n-Butylphthalide at the dosages of 0.3,1.0,and 3.0 mg/kg once a day.The contents of malondialdchyde and super oxide dismutase activity were measured,while the expressions of apoptosis-associated genes and the ultrastructural changes in hippocampus were examined by immunohistnchemisty staining and electron microscope,respectively.Results After irradiation,the content of malondialdehyde and the expression of apoptosis gene bax in rat brain tissue increased while the activity of super oxide dismutase(SOD) and the expression of anti-apoptosis gene bcl-2 decreased.Apoptosis was also observed in the neurons of hippocampus CA1.Compared with irradiation group,the content of malondialdehyde and the expression of bax gene in the DL-3-n-Butylphthalide group wen significantly reduced ( t =-3.89--1.96,2.72-3.48,P ＜ 0.05 ),while the activity of SOD and bcl-2 gene were significantly elevated ( t =2.94-3.76,-3.18--2.08,P ＜ 0.05),and the injury degree of neuron structure in the DL-3-n-Butylphthalide group was slighter than that in the irradiation group.Conclusions DL-3-n-Butylphthalide executes protective effects in a dose-dependent manner againest the radiation injury in rats brain by reducing the induction of malondialdehyde,raising the activity of SOD and inhibiting the generation of apoptosis.
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Objective To observe the effects of Okinawa Habu apoxin protein-1 (OHAP-1) on the proliferation inhibition of rat C6 glioma cells and its mechanisms. Methods MTT colorimetric analysis was used to measure the inhibitory effect of OHAP-1 with different doses(2.5,5.0,and 10.0 mg?L-1) on C6 glioma cells .RT-PCR was used to evaluate the mRNA expressions of bcl-2 and bax genes.The activity of superoxide dismutase (SOD) and the level of maleicdialdehyde (MDA) in the C6 glioma cells were also examined. Results The proliferation of C6 glioma cells was significantly inhibited by different doses of OHAP-1(2.5,5.0,and 10.0 mg?L-1).The inhibitory rate were 49.77%,67.65%,and 76.42%,respectively.The inhibitory rate in 2.5,5.0, and 10.0 mg?L-1 groups were higher than that in control group(P
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Object To study the effect and mechanism of heart beneficial recipe (HBR) on ? amyloid induced neuronal apoptosis Methods In order to establish neurotoxic model, the primary cultured rat hippocampal neurons were treated with 25 ?mol/L aggregated ? amyloid fragment 1 42 (A? 1 42) Neuronal survival was assessed by viable counting after double stained with fluorescein diacetate (FDA) and propidium iodide (PI) Apoptosis of neurons was determined by Hoechst 33258 staining and terminal transferase deoxyuridine nick end labeling (TUNEL) staining The protein expression of Caspase 3 was examined by immunocytochemical SABC method The transcription of mRNAs related to bcl 2, bax, c jun and c fos gene were observed by Northern Blot or RT PCR method Results In the A? 1 42 treated neurons, the number of viable cell was decreased Hoechst 33258 staining showed condensation of nuclear chromatin and nuclear fragmentation TUNEL staining revealed that the number of positive neuron was increased The expression of Caspase 3 protein was elevated The expression of bcl 2 mRNA was decreased, but bax and c jun mRNA were inereased After HBR treatment, the above indexes were improved Conclusion HBR could regulate the expression of apoptosis associated gene and Caspase 3, attenuate the neurotoxic action of A? 1 42 and improve neuronal viability via suppressing apoptotic process