MCI-186 (3-Methyl-1-phenyl-2-pyrazolin-5-one) Attenuated Simulated Ischemia/Reperfusion Injury in Cultured Rat Hippocampal Cells
22
Citation
26
Reference
10
Related Paper
Citation Trend
Abstract:
The reactive oxygen species and Ca2+ overload play a critical role in ischemia/reperfusion (I/R) injury. MCI-186 has potent effects in the brain as a free radical scavenger in ischemia-reperfusion. Acute glucose-oxygen deprivation and subsequent reoxygenation were used to model ischemia/reperfusion injury in cultured hippocampal cells. MCI-186 reduced malondialdehyde level and raised the SOD activity when applied upon reoxygenation in a dose-dependent manner compared with the untreated group. The peak neuroprotective effects occurred at 100 and 300 microM. Intracellular free calcium concentration ([Ca2+]i) was significantly reduced in the 100 microM MCI-186-treated group compared to the untreated group (32.5+/-4.0 versus 50.2+/-3.6, p<0.01). Treatment with 100 microM MCI-186 significantly inhibited the decrease of mitochondria membrane potential after simulated ischemia/reperfusion (204+/-11.6% compared with the untreated group, p<0.01). Cell apoptotic rate was significantly decreased following MCI-186 treatment from 33.7+/-2.3% (untreated group) to 16.6+/-1.4% (100 microM MCI-186 treated group). There was no significantly protective difference between 100 and 300 microM MCI-186. MCI-186 effectively protects neuron injury after simulated ischemia/reperfusion by inhibiting lipid peroxidation, reducing Ca2+ overload, elevating mitochondria membrane potential, and decreasing apoptosis.Hypoxia
Cite
Citations (1)
Ischemia is defined as cell death caused by insufficient perfusion of the tissue due to reduction in arterial or venous blood flow, depletion of cellular energy storages, and accumulation of toxic metabolites. The positive effects of controlled reperfusion are known and are used clinically. But the positive effects of controlled reperfusion on ovarian tissue have not been seen in the literature yet. The biochemical and histopathological comparative investigation of rat ovaries that were experimentally exposed to ischemia (IG), ischemia-reperfusion (I/R), and ischemia-controlled reperfusion (ICR) was aimed. Forty rats were divided into four groups (10 rats per group). First group: 3 h ischemia by vascular clips on ovarian tissue. Second group: 3 h ischemia + 1 h reperfusion. Third group: 3 h ischemia + 1 h controlled reperfusion (on-off method: controlled reperfusion by opening and closing the clips (on/off) in 10-second intervals, for 5 times for a total of 100 seconds). Fourth group: healthy rats. Biochemical (tGSH, MDA, and DNA damage level and SOD activity) and histopathological analysis were performed. The highest glutathione and superoxide dismutase measurements were found in ischemia/controlled reperfusion group among the ischemia or ischemia/reperfusion groups. Similarly the damage indicators (malondialdehyde, DNA damage level and histopathological damage grade) were the lowest in ischemia/controlled reperfusion group. These results indicate that controlled reperfusion can be helpful in minimizing ischemia-reperfusion injury in ovarian tissue exposed to ischemia for various reasons (ovarian torsion, tumor, etc.).
Ovarian torsion
Malondialdehyde
Cite
Citations (35)
Objective: To study NF-κB and IL-6 expression in a rat retina that has been inj ured by ischemia-reperfusion and the effect of β-aescin on its expression.Methods: A retinal model of the rat retina for ischemia-reperfusion was establi s hed. 60 SD rats were divided into two groups: one was an ischemia-reperfusion g r oup and the other was an ischemia-reperfussion and β-aescin group. Each group wa s then divided into sub-groups according to the amount of time after ischemia- re perfusion:1 hour,6 hours,12 hours,24 hours,48 hours,and 72 hours. Each sub -group consisted of 5 rats. NF-κB mRNA and IL-6 mRNA in the rat retina was m easured by the ISH method. Each rat was examined by ERG before being sacrificed.Results: NF-κB and IL-6 began to express at 6 hours after ischemia-reperfusio n i n the ischemia-reperfusion group. The highest level of expression occurred 24 h o urs after injury. In the ischemia-reperfusion and β-aescin group,the NF-κB and IL-6 expressed at 12 hours after ischemia-reperfusion injury and reached the hi ghest level at 24 hours. However,its level was lower than the level for the isc hemia-reperfusion group at every stage(P0.05). The b wave of the ERG in the is chemia-reperfusion group was lower than that for the ischemia-reperfusion and β-aescin group at every stage(P0.05).Conclusion: NF-κB may induce IL-6 and play an important role in ischemia-reperfusion inj ury in the rat retina. The β-aescin may suppress NF-κB activity and protect the retina from injury caused by ischemia-reperfusion.
Erg
Rat model
Cite
Citations (0)
Objective:To evaluate the effect of Polychlorinated Biphenyls(PCB) in cultured hippocampal neuronic cells of rats.Methods:After rats' hippocampal cells were cultured with different PCB, MTT was used to observe the growth and development of hippocampal cells.Results:It was obvious that hippocampal neuronic cells was inhibited in the highest groups of PCB,10 -4 group was apparently lower than that of control group(P0.01);10 -7 and 10 -6 groups were lower than that of control group(P0.05);The live rate of cell was reduced.Conclusion:PCB had strong nerve toxicity to hippocampal neuronic cells.
Nerve cells
Cite
Citations (0)
[Objective]To study the IL-6 express in rat's retina which injuried by ischemia-reperfusion and the effect of β-aescin on its expression. The model of rat's retina ischemia-reperfusion was employed. 60 SD rats were devided into two groups, one was ischemia-reperfusion group, the other was ischemia-reperfusion andβ-aescin group. Every group was devided into 1 hour, 6 hour, 12 hour, 24 hour, 48 hour and 72 hour groups. Every group had 5 rats. IL-6 mRNA was measured by ISH method in rat's retina. Every rat was examinated ERG before executed. IL-6 began to express at 6 hours after ischemia-reperfusion in ischemia-reperfusion group. It expressed most at 24 hours after ischemia-reperfusion injury. In ischemia-reperfusion and β-aescin group, IL-6 expressed at 12 hours after ischmia-reperfusion injury and reached the hightest level was lower than ischemia-reperfusion group at every stage (P 0.05). The a wave of ERG of ischemia-reperfusion group was lower than ischemia-reperfusion and β-aescin group at every stage (P 0.05). [Conclusion] IL-6 take important role in rat's retina ischemia-reperfusion injury, the β-aescni may suppress the activity of IL-6 and relieve the retina injury from the ischemia-reperfusion.
Erg
Rat model
Cite
Citations (0)
Objective:The retina ischemia-reperfusion injury is caused by many factors. A lot of cell factors take part in it. Many researches suggest MCP-1 has special effect on leukocyte and lymphocyte.The research try to study the effect of MCP-1 in rat's retina ischemia-reperfusion injury.Methods:To employ the rat's retina ischemia-reperfusion model and use SABC method to test the expression of MCP-1 on retina.Results:There was no MCP-1 expressed in retina after ischemia-reperfusion injury for one hour. MCP-1 began to express in retina after ischemia-reperfusion injury for six hours, and expressed at most after ischemia-reperfusion injury for 24 hours. Then it began to decrease in 48 hours after ischemia-reperfusion injury, but it still expressed in retina in seventy-two hours after ischemia-reperfusion injury.Conclusions:MCP-1 plays an important role in rat's retina ischemia-reperfusion injury.
Cite
Citations (0)
Objective To observe the protective effect of brain-derived neurotrophic factor(BDNF) on Aβ25-35-induced primarily cultured hippocampal neuron injury.Methods Hippocampal cells taken from new-born Wistar rats were incubated in vitro,into which different concentrations of BDNF and aggregated Aβ25-35 were added to act on the cultured hippocampal neurons.Effect of BDNF on the survival rate of hippocampal neurons and apoptosis of hippocampal cells induced by Aβ25-35 was observed by MTT and Hoechst 33342 staining,respectively.Results The damage of hippocampal cells was less severe in BDNF treatment group than in Aβ25-35 model group,and the hippocampal cells grew well under microscope.MTT showed that the survival rate of hippocampal cells increased with the increased concentration of BDNF.Hoechst 33342 staining showed that the apoptosis rate of hippocampal cells decreased with the increased concentration of BDNF,which was lower in BDNF treatment group than in Aβ25-35 model group(P0.01).Conclusion BDNF can protect the cultured hippocampal neurons against injury induced by Aβ25-35 due to its neurotrophic activity.
MTT assay
Cite
Citations (0)
Objective To investigate the effect of palm oil(PO) on the volume of the infarction,the expression of Bcl-2 and Bax protein following focal cerebral ischemia/reperfusion in rats,and explore the protective effect of PO on focal cerebral ischemia/reperfusion and the underlying mechanism.Methods The acute focal cerebral ischemia/reperfusion models were established with suture emboli.Healthy male Sprague-Dawley rats were randomly divided into four groups: normal control group,sham group,IR group and PO group.There were 12 rats in each of the normal control group and the sham group.The IR group and PO group were further subdivided into subgroups and sacrificed 2 h,6 h,12 h,24 h,72 h and 7 d after ischemia/reperfusion(n=12).The volume of the infarction was observed by the TTC method;and the expression of Bcl-2 and Bax was determined by Western blotting to observe the protective effect of PO.Results ① TTC staining: there was no region of ischemia/reperfusion injury in the normal control group and the sham group.There was no region of ischemia/reperfusion injury in IR group and PO group 2 h after ischemia/reperfusion.At the time points of 6 h,12 h,24 h,72 h and 7 d after ischemia/reperfusion,there were statistical differences in mass percentage of the infracted regions between the PO group and the IR group(P0.05),and mass percentage of the infracted cerebral regions in the PO group was reduced as compared to the IR group.② Western-blotting: From the time point of 6h after reperfusion,in both PO group and IR group,the expression of Bcl-2 and Bax increased with time in the ischemia penumbra with peak expression at 12 h,and then decreased.The expression of Bax reached the peak at 24 h,and then decreased.Western-blotting analysis showed a gradual increase in Bcl-2 expression(P0.05) and a gradual decrease in Bax expression(P0.05) in PO group at each time point(6 h,12 h,24 h and 72 h after ischemia/reperfusion),compared with IR group.Conclusions ① PO can reduce the region of ischemia injury following focal cerebral ischemia/reperfusion injury;② PO can protect nerve cells by increasing the expression of Bcl-2 and decreasing the expression of Bax,following the cerebral ischemia/reperfusion injury.
Cite
Citations (0)
Objective:To investigate the protective effects of naoyikang on D-gal-induced injury in cultured hippocampal neurons in neonatal SD rat.Methods: By way of seropharmacology to collect the sera containing Naoyikang.Cultured hippocampal neurons were treated with D-gal.The protective effect of naoyikang were evaluated by cell morphology and colorimetric MTT assay.Results:Naoyikang can significantly increased the number of hippocampal neurons.Conclusion:Naoyikang can protect hippocampal neurons injuried from D-gal-induced injury.
MTT assay
Cite
Citations (0)