The advanced retrieval of VIP and Wanfang is similar to the standard retrieval in cnKI. When searching, it is suggested to put melatonin and apoptosis under the title field and the protection function in the subject field.
The title information of VIP download is as follows:
1/5
Effects of melatonin on NF-KB expression and apoptosis in substantia nigra of Parkinson's disease model in vitro.
Author Xing,,, Wang,, Hong Can
China Journal of Neuroimmunology and Neurology. 2008 ( 1)。
Department of Neurology, First Affiliated Hospital of Henan Weihui Xinxiang Medical College 453 100 Department of Neurology, Affiliated Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan Mental Health Center, Hubei 430022 Department of Neurology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052.
ISSNNo。 1006-2963
CNNO . 1 1-3552/r
The collection number is 98536X.
Parkinson's disease, 6- hydroxydopamine apoptotic nuclear factor -kB p65 in substantia nigra.
Classification number R742.5
Objective To study the effect of melatonin (MT) on Parkinson's disease (PD) model induced by 6- hydroxydopamine (6-OHDA). Methods 14 rats were divided into sham operation group, MT group and control group. MT group was injected intraperitoneally for 3 days, and the other two groups were injected with the same amount of normal saline. Then brain slices from MT group and control group were incubated in artificial cerebrospinal fluid containing 6-OHDA for 2 hours. TUNEL method and immunohistochemical technique were used to observe the apoptosis number of substantia nigra cells and detect the expression of NF-kBp65 in substantia nigra. Results There was no obvious apoptosis in substantia nigra in sham operation group, and the apoptosis in substantia nigra in MT group was significantly lower than that in control group, and the expression of NF-KBP65 in substantia nigra was also reduced, with statistical significance. Conclusion MT has protective effect on PD model in vitro, and its mechanism may be anti-apoptosis.
2/5
Effect of melatonin on apoptosis of megakaryocytes and its mechanism
Author Zhou,,,, Yang Mo
Journal of third military medical university. 2008( 18)
Department of Hematology, Children's Hospital Affiliated to Chongqing Medical University, Department of Hematology, Chengdu Children's Hospital, Chongqing 4000 14, Chengdu 6 100 14 Department of Pediatrics and Adolescent Science, Li Ka-shing Medical College.
ISSNNo。 1000-5404
CNNO . 50- 1 126/r
The collection number is 92 156X.
Melatonin; Apoptosis of megakaryocyte AKT ERK
Classification number R329.28 R33 1. 14.
Objective To explore the effect of melatonin on the apoptosis of megakaryocytes and its mechanism. Methods Serum was removed to induce the apoptosis of megakaryocyte cell line CHRF-288- 1 1. With or without Mel***, the apoptosis indexes: Annexin V/PI, Caspase-3 and JC- 1 were detected by flow cytometry, and compared with normal group and TPO group. At the same time, signal paths AKT and ERK 1/2 are detected to understand the mechanism of their participation in protection. Results After 72h of MEL 200 nmol/L treatment, the expressions of Annexin V/PI, Caspase-3 and JC- 1 in CHRF cells were significantly lower than those in the control group, from 42.9%, 29.5% and 47.7% to 3 1.7% (P < 0.05) and 2650, respectively. Among them, the expression of JC- 1 was statistically significant compared with that of TPO group (20.7 5.2)%, but the expression of annexin V/PI and Caspase-3 was not statistically significant compared with TPO group. After adding Mel, the levels of phosphorylated AKT and ERK 1/2 in CHRF cells increased significantly, from (5.9 0.1)% and (6. 1.4)% to (9.5 0.1)%, respectively. Conclusion Mel can inhibit the apoptosis of megakaryocytes, and its protective mechanism may play a role through AKT and ERK signaling pathways.
3/5
Protective effect of melatonin on apoptosis of microvascular cells in diabetic retinopathy rats
Author Xia Peijin, Song, Li, Shi, Zhimin,
Academic journal of second military medical university. 2007(7)
Department of Endocrinology, Changzheng Hospital, Second Military Medical University, 200003 Department of Endocrinology, Zhejiang Provincial People's Hospital, Hangzhou 3 100 14.
ISSNNo。 0258-879X
CNNONo。 3 1- 100 1/R
Collection number is 9 1242X.
Protective effect of diabetic retinopathy; Rat model; Apoptosis; Microvessels; Melatonin; Immunohistochemical method; streptozotocin
Classification number R587.2
Objective: To observe the protective effect of melatonin on apoptosis of microvascular cells in diabetic retinopathy rats. Methods: Diabetic rat model was induced by streptozotocin (60 mg/kg). After the model was successfully established, it was randomly divided into three groups according to body weight and blood sugar: diabetes group, low-dose Mel group [0.5 mg/(kg d)] and high-dose Mel group [10 mg/(kg d)]. Another normal control group (7 rats) was set up. After intervention 12 weeks, the expressions of NF-κB, bcl-2 and Bax in retina of rats in each group were detected by immunohistochemical method. The positive area was measured by image analyzer and its expression was calculated.
4/5
Dynamic changes of myocardial apoptosis during donor heart preservation in rats and the protective effect of melatonin
Author Gao, Pan Tiecheng, Yang,
Journal of traditional chinese medicine. 2004(2)
Department of Cardiology, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030.
ISSNNo。 100 1- 1668
CNNO . 1 1-2 166/r
Collection number. 90 1 15X
Keywords organ preservation; Rat heart transplantation
Classification number R654.2
Objective To investigate the dynamic changes of cardiomyocyte apoptosis and the protective effect of melatonin during donor heart preservation in rats. Methods 80 Wistar rats were randomly divided into experimental group and control group. In the experimental group, melatonin (0. 1mmol/L) was added to 4℃StThomas solution to preserve the rat heart. The control group was only preserved with StThomas solution. Eight donor hearts were preserved for 4, 8, 12, 2 4 and 36 hours, and apoptosis was detected by TUNEL staining. The percentage of cardiomyocyte apoptosis positive cells in the total number of cardiomyocytes was used as the cardiomyocyte apoptosis index. Results With the prolongation of preservation time, the number of apoptotic cardiomyocytes increased significantly, and the differences at each time point were statistically significant (P < 0.01). Apoptosis index of myocardial cells in experimental group was significantly lower than that in corresponding control group (7.68%1.04% vs 24.37%1.23%, P < 0.06；; 8.2 7% 1. 1.7% vs 3 5.73% 1.98%, P<0 .0 1; 10.14%1.2% vs 42.85% 2.3% p < 0 .0 1; 12.31%1.54% versus 58.3 7% 3. 12%, P<0 .0 1; 14.53% 1.89% vs 79.65% 4. 16%, P<0 .0 1) ...
5/5
Protective effect of melatonin on apoptosis of PC 12 cells induced by oxygen free radicals
Author Fu Kong Xiaoyan Zeng Jiping Cui Xing
Journal of Shandong University: Medical Edition.2004 (6)
Institute of Biochemistry and Molecular Biology, School of Medicine, Shandong University, Shandong Center for Disease Control and Prevention, Jinan 2500 12, Shandong 250000.
ISSNNo。 167 1-7554
CNNOno。 37- 1390/R
Collection number. 954 13A
Reactive oxygen species; Apoptosis; Alzheimer's disease
Classification number R74 1.02
Objective: To explore the role and possible mechanism of oxygen free radicals in Alzheimer's disease, and to evaluate the clinical application value of melatonin. Methods: PC 12 cells were treated with xanthine/xanthine oxidase system (X/XO), a superoxide radical generation system, and the morphological changes were observed after melatonin antagonism. Cell survival rate was detected by MTT assay, apoptosis was analyzed by DNA electrophoresis and flow cytometry, and the expression of apoptosis-related genes bcl-2 and bax was detected by RT-PCR. Results: After X/XO treatment, PC 12 cells showed characteristic apoptosis changes, and the apoptosis rate increased. Electrophoresis showed that DNA ladder and apoptosis-related gene bax were up-regulated. And 10-5m melatonin can promote apoptosis. Conclusion: Oxygen free radicals can induce neuronal apoptosis, thus promoting AD, and its mechanism is related to the increased expression of apoptosis-related gene Bax. Melatonin can slow down neuronal apoptosis and can be used for clinical prevention and treatment.