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Oxido-reduction disturbance may be involved in the pathogenesis of AMD. There is a significantly decreased antioxidant capacity in AMD patients.

Background: Temporal lobe epilepsy (TLE) is the most common type of intractable epilepsy in humans, and it is often accompanied by cognitive impairment. In this study, we examined the effects of (-)-Epigallocatechin-3-gallate (EGCG) after SE on behavior in the rat lithium-pilocarpine model of TLE. Material/Methods: The rats were randomly divided into 3 groups: (1) the control group, in which 12 rats received no treatment; (2) the epilepsy (EP) group, in which 15 rats were treated with saline after status epilepticus (SE); and (3) the EP+EGCG group, in which 15 rats were treated with EGCG (25 mg/kg/d, intraperitoneal) after SE. The SE model was induced with lithium chloride-pilocarpine, and electroencephalography and a high-definition camera were used to monitor SRS. The Morris water maze test and hippocampal late-phase long-term potentiation (L-LTP) recordings were used to evaluate cognitive impairment, and TLR4, NF-kB, and IL-1b levels were determined using Western blot analysis. Results: We concluded that EGCG treatment after SE (1) markedly reduced SRS frequency in pilocarpine-treated rats, (2) improved epilepsy-induced cognitive impairment and reversed epilepsy-induced synaptic dysfunction in L-LTP in vivo, (3) protected hippocampal neurons from damage after SRS, and (4) significantly attenuated the increase in TRL-4 and IL-1b hippocampal levels. The above findings clearly show that EGCG exerts antiepileptogenesis and neuroprotective effects on pilocarpine-induced epilepsy. Conclusions: We found that EGCG can suppress seizures and inhibit hippocampal neuronal apoptosis, as well as improving cognitive function of epileptic rats. Our findings suggest that EGCG may a novel adjuvant therapeutic approach in epilepsy by improving epileptic behavior and cognitive dysfunction.

Previous studies have revealed significant roles for long noncoding RNA (lncRNA) in the tumorigenesis, metastasis and invasion of various tumors, including cervical cancer. The present study aimed to investigate the potential roles of lncRNA colon cancer associated transcript 1 (CCAT1) in the metastasis and invasion of cervical cancer, and to reveal the potential underlying mechanism. The mRNA expression of lncRNA CCAT1 in cervical cancer tissue was measured using the reverse transcription‑quantitative polymerase chain reaction, and the association between lncRNA CCAT1 and the metastasis of cervical cancer was analyzed. The effects of lncRNA CCAT1 expression on HeLa cell viability, and migration and invasion were also analyzed by MTT and Transwell assays. The results demonstrated that lncRNA CCAT1 was highly expressed in the cervical cancer tissue compared with the adjacent normal tissue. High expression of lncRNA CCAT1 was positively associated with tumor size, and there was correlation between high lncRNA CCAT1 expression and a poor survival rate of cervical cancer. The cell viability, and migratory and invasive abilities were suppressed by silencing CCAT1. The results of the present study indicate that lncRNA CCAT1 was highly expressed in cervical cancer, and may serve important roles in promoting the progression and metastasis of cervical cancer.