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Objective:To study the influence of G protein-coupled estrogen receptor 1 (GPER1) specific agonist G1 and antagonist G2 in epilepsy susceptibility of temporal lobe epileptic rats.Methods:Sixty rats were randomly divided into control group, G1 treatment group and G15 treatment group ( n=20). Rats in the latter two groups were intraperitoneally injected with GPER1 agonist G1 (10 μg) or antagonist G15 (40 μg) for a consecutive 12 d. Lithium chloride pilocarpine epilepsy models were prepared in the 3 groups. The behavior manifestations of these rats were observed within 1 h of intraperitoneal injection of pilocarpine; Racine grading was used to evaluate the severity of epileptic seizures every 5 min; the latency of epileptic seizures (Racine grading IV) and epileptic seizure grading at different time points in the 3 groups were compared. The EEG monitoring was performed to these rats, and EEG data were recorded from 10 min before pilocarpine injection to 2 h after pilocarpine injection; EEG time-frequency was analyzed by Fast-Fourier transform (FFT); distribution of brain electrical energy and changes of θ and α wave energy during 20 min of epileptic status were compared among the 3 groups. Results:(1) As compared with that in the control group and G1 treatment group, the latency of epileptic seizures in the G15 treatment group was significantly shortened ( P<0.05); 15 and 20 min after pilocarpine injection, the epileptic seizure grading of rats in G1 treatment group was statistically lower than that in control group ( P<0.05); 15-35 min after pilocarpine injection, the epileptic seizure grading of rats in G15 treatment group was significantly higher than that in control group ( P<0.05). (2) As compared with those in the control group, rats in the G1 treatment group had smaller brain wave amplitude, while the rats in the G15 treatment group had earlier seizure time, larger brain wave amplitude and higher frequency. There were no obvious changes in the amount of brain electrical energy between the G1 treatment group and control group; while the amount of brain electrical energy in the G15 treatment group 2 h after pilocarpine injection was higher than that in the control group. As compared with those in the control group and G1 treatment group, the θ and α wave energy values of rats in the G15 treatment group were significantly increased within 20 min of epileptic status ( P<0.05). Conclusion:Activation level of GPER1 might be associated with susceptibility to epileptic seizures, and specific inhibition of GPER1 activation can enhance the susceptibility to epilepsy and increase the energy values of specific frequency bands during epilepsy.
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Objective To study the role and mechanism of orexin A in cell viability of Alzheimer's disease (AD) cell model PC12. Methods PC12 cells were treated with 0, 10, 20, 30, 40 and 50 μmol/L Aβ25-35 for 24 h, and then, cell viability was measured by MTT to confirm which concentration was the suitable one to establish the AD cell models. (1) AD cell models were treated with 0, 0.01, 0.1, 1 and 2μmol/L orexin A for 24 h, and then, 30μmol/L Aβ25-35 was added for 24 h; MTT assay was used to determine the cell viability to conform the suitable concentration of orexin A. (2) Inverted phase contrast microscope was employed to observe the morphology changes of PC12 cells from the control group, 30 μmol/L Aβ25-35 treatment group, and 0.01 μmol/L orexin A+30 μmol/L Aβ25-35 treatment group. (3) The PC12 cells were given pretreatment of orexin A receptor inhibitor SB408124 for 2 h, and cell viability was detected. Results (1) Aβ25-35 at concentration 30μmol/L was the suitable one to establish the AD cell models;after being pretreated with different concentrations of orexin A, the cell viability showed significant differences (F=27.120, P=0.000), and 0.01μmol/L orexin A was the suitable concentration. (2) Some of the cells from the 30μmol/L Aβ25-35 treatment group had breaking-off of protuberance and damaged soma;cells from 0.01μmol/L orexin A+30μmol/L Aβ25-35 treatment group had breaking-off of protuberance, and the degree of damaged soma was eased as compared with that in the 30μmol/L Aβ25-35 treatment group. (3) If the cell viability of the control group was 100％, cell viability of orexin A receptor inhibitor group was 109.10％±0.36％, which was significantly decreased as compared with that in the 0.01 μmol/L orexin A pretreated group (117.24％±2.72％, P<0.05). Conclusion Orexin A can improve the cell viability via combination of its specific receptor; orexin A and its specific receptor may be new targets for prevention and cure of AD.
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Objective To study the relationship between the health?related quality of life and Graves′ophthalmopathy quality of life(GO?QOL)in Graves′ophthalmopathy(GO)patients. Methods A total of 44 GO patients were recruited for the study and investigated with SF?36 and GO?QOL questionnaires. In addition,the thyroid function and related antibodies were also detected. Results The scores of SF?36 and GO?QOL were higher in the patients over 45 years than those under 45 years(P<0.05). GO?QOL score was lower in the patients with thyroid stimulating hormone recep?tor antibody higher than 10 IU/mL(P<0.05). The scores of SF?36 and GO?QOL were obviously higher in the patients who had a clinical activity score above 3(P<0.01). Conclusion GO?QOL is a better and more specific questionnaire for GO patients.