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melatonin combined with exercise cannot alleviate cerebral injury in a rat model of focal cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2012年第13期7卷 993-999页

作者： Seunghoon Lee Jinhee Shin Minkyung Lee Yunkyung Hong Sang-Kil Lee Youngjeon Lee Tserentogtokh Lkhagvasuren Dong-Wook Kim Young-Ae Yang Kyu-Tae Chang Yonggeun Hong Department of Rehabilitation Science in Interdisciplinary Ph.D.Program Inje UniversityGimhae 621-749Republic of Korea Cardiovascular & Metabolic Disease Center College of Biomedical Science & EngineeringGimhae 621-749Republic of Korea Department of Smart Foods & Drugs School of Food & Life SciencesInje UniversityGimhae 621-749Republic of Korea Department of Pharmaceutical Engineering College of EngineeringInje UniversityGimhae 621-749Republic of Korea National Primate Research Center Korea Research Institute of BiotechnologyOchang 363-883Republic of Korea

Previous studies have demonstrated that melatonin combined with exercise can alleviate secondary damage after spinal cord injury in rats. Therefore, it is hypothesized that melatonin combined with exercise can also alleviate ischemic brain damage. In this study, adult rats were subjected to right middle cerebral artery occlusion after receiving 10 mg/kg melatonin or vehicle subcutaneously twice daily for 14 days. Forced exercise using an animal treadmill was performed at 20 m/min for 30 minutes per day for 6 days prior to middle cerebral artery occlusion. After middle cerebral artery occlusion, each rat received melatonin combined with exercise, melatonin or exercise alone equally for 7 days until sacrifice. Interestingly, rats receiving melatonin combined with exercise exhibited more severe neurological deficits than those receiving melatonin or exercise alone. Hypoxia-inducible factor la mRNA in the brain tissue was upregulated in rats receiving melatonin combined with exercise. Similarly, microtubule associated protein-2 mRNA expression was significantly upregulated in rats receiving melatonin alone. Chondroitin sulfate proteoglycan 4 （NG2） mRNA expression was significantly decreased in rats receiving melatonin combined with exercise as well as in rats receiving exercise alone. Furthermore, neural cell loss in the primary motor cortex was significantly reduced in rats receiving melatonin or exercise alone, but the change was not observed in rats receiving melatonin combined with exercise. These findings suggest that excessive intervention with melatonin, exercise or their combination may lead to negative effects on ischemia/reperfusion-induced brain damage.

关键词： wfocal cerebral ischemiaJreperfusion melatonin exercise neurological function brain tissue loss microtubule associated protein-2 chondroitin sulfate proteoglycan 4 NG2 hypoxia-inducible factor1 alpha neural regeneration

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melatonin attenuates hepatic ischemia-reperfusion injury in rats by inhibiting NF-κB signaling pathway

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Hepatobiliary & Pancreatic Diseases International 2021年第6期20卷 551-560页

作者： Yao Gao Zhi-Tao Li Li Jin Jie Lin Zheng-Lei Fan Zhong Zeng Han-Fei Huang Organ Transplantation Center the First Affiliated Hospital of Kunming Medical UniversityKunming 650032China

Background:The sterile inflammatory response is one of the key mechanisms leading to hepatic ischemia-reperfusion injury.melatonin has been shown to prevent organ injuries,but its roles in the inflammatory response after hepatic ischemia-reperfusion injury have not been fully explored,especially in late ischemia-reperfusion injury.The present study aimed to investigate the roles and possible mechanisms of melatonin in the inflammatory response after hepatic ischemia-reperfusion injury.Methods:Sixty Sprague-Dawley rats were randomly divided into a sham group,ischemia-reperfusion injury group(I/R group),and melatonin-treated group(M+I/R group).The rats in the I/R group were subjected to 70%hepatic ischemia for 45 min,followed by 5 or 24 h of reperfusion.The rats in the M+I/R group were injected with melatonin(10 mg/kg,intravenous injection)15 min prior to ischemia and immediately before reperfusion.Serum and samples of ischemic liver lobes were harvested for future analysis,and the 7-day survival rate was assessed after hepatic ischemia-reperfusion surgery.Results:In comparison with the I/R group,the M+I/R group showed markedly decreased expression levels of inflammatory cytokines(IL-6 and TNF-α)and numbers of apoptotic hepatocytes(Pmelatonin downregulated the activity of the NF-κB signaling pathway in the early and late stages of hepatic ischemia-reperfusion injury,alleviated the inflammatory response,protected the liver from ischemia-reperfusion injury,and increased the survival rate.

关键词： melatonin Ischemia-reperfusion injury Inflammation NF-κB Liver

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melatonin-selenium nanoparticles protects liver against immunological injury induced by bacillus Calmette-Guérin and lipopolysaccharide

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Acta Pharmacologica Sinica 2005年第6期26卷 745-752页

作者： Hua WANG, Wei WEI~3, Sheng-yi ZHANG~2, Yu-xian SHEN, Ni-ping WANG, Li YUE, Shu-yun XU Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, China ~2Department of Chemistry, Anhui University, Hefei 230039, China. Institute of Clinical Pharmacology Anhui Medical University Hefei China Department of Chemistry Anhui University Hefei China

Aim: melatonin-selenium nanoparticle (MT-Se), a novel complex, was synthesized by preparing selenium nanoparticles in a melatonin medium. The present investigation was designed to determine the protective effects of MT-Se against immunological liver injury in mice induced by bacillus Calmette-Guerin (BCG)/ lipopolysaccharide (LPS). Methods: The model of immunological liver injury in mice was prepared. The levels of alanine aminotransferase, aspartate aminotransferase, nitric oxide (NO) in serum, malondialdehyde content, superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) activities in a liver homo-genate were assayed by spectrophotometry. The content of tumor necrosis fac-tor (TNF) and interleukin-1 (IL-1) were determined by ELISA. The splenocyte proliferation was assayed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetra-zolium bromide (MTT) dye reduction. Meanwhile, a hepatic pathological examination was observed. Results: In the BCG/LPS-induced hepatic injury model, MT-Se administered at doses of 5,10, or 20 mg/kg to the BCG/LPS-treated mice for 10 d significantly reduced the increase in serum aminotransferase, reduced the severe extent of hepatic cell damage and the immigration of inflammatory cells. It also attenuated the increase in the content of thiobarbituric acid-reactive substances and enhanced the decrease in activities of SOD and GSH-px. In contrast, the treatment with MT-Se suppressed the increase in NO level in both the serum and liver tissue. Furthermore, MT-Se significantly lowered an increase in TNF and IL-1 levels in the liver and inhibited the production of TNF and IL-1 by peritoneal macrophages. A downregulation effect of MT-Se on splenocyte proliferation was also observed. Conclusion: MT-Se showed a hepatic protective action on immunological liver injury in mice.

关键词： melatonin selenium liver superoxide dismutase glutathione peroxidase nitric oxide tumor necrosis factor interleukin-1

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melatonin modifies SOX2^+ cell proliferation in dentate gyrus and modulates SIRT1 and MECP2 in long-term sleep deprivation

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Neural Regeneration Research 2019年第10期14卷 1787-1795页

作者： Alan Hinojosa-Godínez Luis F. Jave-Suarez Mario Flores-Soto Alma Y. Gálvez-Contreras Sonia Luquín Edith Oregon-Romero Oscar González-Pérez Rocio E. González-Castaneda Laboratorio de Microscopía de Alta Resolución Departamento de NeurocienciasCentro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico Laboratorio de Neurociencias Facultad de PsicologíaUniversidad de ColimaColimaMéxico División de Inmunología Centro de Investigación Biomédica de OccidenteInstituto Mexicano del Seguro SocialGuadalajaraMéxico División de Neurociencias Centro de Investigación Biomédica de OccidenteInstituto Mexicano del Seguro SocialGuadalajaraMéxico Instituto de Investigación en Ciencias Biomédicas (IICB) Departamento de Biología Molecular y GenómicaCentro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico Unidad de Atención en Neurociencias Departamento de Neurociencias. Centro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico

melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult hippocampus.However,this effect has not been observed in long-term sleep deprivation.The precise mechanism exerted by melatonin on the modulation of neural stem cells is not entirely elucidated,but evidence indicates that epigenetic regulators may be involved in this process.In this study,we investigated the effect of melatonin treatment during a 96-hour sleep deprivation and analyzed the expression of epigenetic modulators predicted by computational text mining and keyword clusterization.Our results showed that the administration of melatonin under sleep-deprived conditions increased the MECP2 expression and reduced the SIRT1 expression in the dentate gyrus.We observed that let-7 b,mir-132,and mir-124 were highly expressed in the dentate gyrus after melatonin administration,but they were not modified by sleep deprivation.In addition,we found more Sox2^+/5-bromo-2’-deoxyuridine(BrdU)^+cells in the subgranular zone of the sleep-deprived group treated with melatonin than in the untreated group.These findings may support the notion that melatonin modifies the expression of epigenetic mediators that,in turn,regulate the proliferation of neural progenitor cells in the adult dentate gyrus under long-term sleep-deprived conditions.All procedures performed in this study were approved by the Animal Ethics Committee of the University of Guadalajara,Mexico(approval No.CI-16610)on January 2,2016.

关键词： sleep-deprivation melatonin microRNA neurogenesis Sirtuin 1 SIRT1 methyl-CpG-binding protein 2 MECP2 epigenetic text-mining mir-9 let-7b

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melatonin for an obese child with MC4R gene variant showing epilepsy and disordered sleep: A case report

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World Journal of Clinical Cases 2021年第11期9卷 2688-2695页

作者： Wen-Rong Ge Lin Wan Guang Yang Department of Pediatrics Beijing Friendship HospitalCapital Medical UniversityBeijing 100000China Department of Pediatrics The First Medical Center of Chinese PLA General HospitalBeijing 100853China

BACKGROUND Abnormalities in the melanocortin receptor 4(MC4R)gene often lead to obesity,but are rarely associated with other conditions such as epilepsy and sleep disorder.CASE SUMMARY Here,we present a case of a male obese child with a heterozygous variant in MC4R(c.494G>A,p.Arg165Gln)inherited from his father,who presented with disordered sleep and abnormal facial movements.Examination through melatonin rhythm testing and electroencephalography led to a diagnosis of sleep disorder and epilepsy,as his melatonin rhythm was markedly distorted and the electroencephalography revealed epileptic discharges.He received treatment with an antiepileptic drug;however,the therapy was ineffective and the sleep disorder appeared to be deteriorating.Subsequently,we initiated adjuvant treatment with melatonin.Upon re-examination,his body mass index had decreased,the sleep disturbance had resolved,and his seizures were well controlled.Electroencephalography review was normal,and a typical melatonin rhythm was restored.CONCLUSION We concluded that,in addition to causing obesity,abnormalities in the MC4R gene may contribute to the development of sleep disorders and epilepsy,and that melatonin can be used as an adjuvant therapy to alleviate these symptoms.

关键词： Melanocortin receptor 4 Obesity Sleep disorders Epilepsy melatonin Case report

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melatonin and/or rowatinex attenuate streptozotocin-induced diabetic renal injury in rats

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The Journal of Biomedical Research 2019年第2期33卷 113-121页

作者： Tarek K Motawi Samia A Ahmed Manal A Hamed Shohda A El-Maraghy Wessam M Aziz Biochemistry Department Faculty of Pharmacy Cairo University Therapeutic Chemistry Department National Research Centre

The study aimed to explore the prophylactic effect of melatonin, rowatinex; a naturally occurring renal drug, and its combination on diabetic nephropathy in type 2 diabetic rats. Diabetes was induced by intraperitoneal injection of a single dose of streptozotocin(50 mg/g body weight). Three days before diabetes induction, rats were daily treated with melatonin, rowatinex and their combination continuously for 8 weeks. Evaluation was done through measuring blood urea nitrogen(BUN), serum uric acid, serum creatinine, urine creatinine, creatinine clearance, nitric oxide(NO), malondialdehyde(MDA), superoxide dismutase(SOD), glutathione(GSH), total antioxidant capacity(TAC),kidney injury molecule-1(KIM-1), heat shock protein-70(HSP-70), caspase-3, transforming growth factor β1(TGFβ1), DNA degradation by the comet assay and total protein contents. Histopathologic study was also done for the kidney and the pancreas. Drastic changes in all measured parameters of the diabetic rats were observed. Treatment with melatonin and rowatinex showed amelioration to variable degrees. In conclusion, melatonin showed the most potent effect on protecting rats from deleterious action of diabetic nephropathy followed by its combination with rowatinex.

关键词： diabetic nephropathy melatonin rowatinex histopathology

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melatonin Ameliorates Liver Fibrosis Induced by Carbon Tetrachloride in Rats via Inhibiting TGF-β1/Smad Signaling Pathway

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Current Medical Science 2018年第2期38卷 236-244页

作者： Yu-rong WANG Ru-tao HONG Yuan-yuan XIE Jian-ming XU Department of Gastroenterology First Affiliated Hospital of Anhui Medical University Key Laboratory of DigestiveDisease of Anhui Province Hefei 230022 China

melatonin has been reported to inhibit hepatic fibrosis and the mechanism may be correlated to its anti-oxidant effect. Nevertheless, the mechanism is not completely identified. This study was conducted to investigate the effects of melatonin on TGF-β1/Smad signaling pathway in liver fibrosis in rats. The liver fibrosis model was made by the subcutaneous injection of CC14. The liver pathology changes were detected using hematoxylin and eosin （H＆E） staining and Van Gieson （VG） staining. Serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） activities were measured with an autoanalyzer. Glutathione peroxidase （GPx） activities and levels of malondialdehyde （MDA） and hydroxyproline （Hyp） in liver were evaluated by spectrophotometry. Expression levels of TGF-β1, Smad2/3, phosphorylated Smad2/3 （p-Smad2/3） and Smad7 in liver were detected by immunohistochemistry and Western blot analysis. Results showed that melatonin suppressed CC14-induced liver fibrosis, along with an improvement in histological changes, significant decreases in pathologic grading sores and obvious decreases in Hyp levels in liver. melatonin improved liver function indicated by decreased serum ALT and AST activities. In addition, melatonin exerted its anti-oxidant effects, as supported by decreased MDA levels and increased GPx activities in liver. Furthermore, melatonin inhibited TGF-β1/Smad pathway, as evidenced by decreased TGF-β1, Smad2/3 and p-Smad2/3 expression and increased Smad7 expression in liver. In conclusion, melatonin may suppress CCl4-induced hepatic fibrosis in rats via inhibiting TGF-β1/Smad pathway. It is possible for melatonin to be a potential reagent to treat and cure liver fibrosis.

关键词： melatonin liver fibrosis TGF-β1 Smad

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melatonin Protects N2a against Ischemia/Reperfusion Injury through Autophagy Enhancement

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第1期30卷 1-7页

作者：国艳春王剑飞王忠强杨易王西明段秋红 Department of Biochemistry and Molecular Biology School of Basic Medical SciencesTongji Medical CollegeHuazhong University of Science and Technology Department of Emergency Medicine Wuhan General Hospital of Guangzhou Command

Researches have shown that melatonin is neuroprotectant in ischemia/reperfusion-mediated injury.Although melatonin is known as an effective antioxidant,the mechanism of the protection cannot be explained merely by antioxidation.This study was devoted to explore other existing mechanisms by investigating whether melatonin protects ischemia/reperfusion-injured neurons through elevating autophagy,since autophagy has been frequently suggested to play a crucial role in neuron survival.To find it out,an ischemia/...

关键词： melatonin autophagy ischemia/reperfusion rapamycin 3-MA LC3 Beclin1 PKB N2a

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melatonin, a novel selective ATF-6 inhibitor, induces human hepatoma cell apoptosis through COX-2 downregulation

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World Journal of Gastroenterology 2017年第6期23卷 986-998页

作者： Li-Jia Bu Han-Qing Yu Lu-Lu Fan Xiao-Qiu Li Fang Wang Jia-Tao Liu Fei Zhong Cong-Jun Zhang Wei Wei Hua Wang Guo-Ping Sun Department of Oncology the First Affiliated Hospital of Anhui Medical University Department of Pharmacy the First Affiliated Hospital of Anhui Medical University Institute of Clinical Pharmacology Anhui Medical University Institute for Liver Diseases of Anhui Medical University

AIM To clarify the mechanisms involved in the critical endoplasmic reticulum(ER) stress initiating unfolded protein response pathway modified by melatonin.METHODS Hepatoma cells, Hep G2, were cultured in vitro. Flow cytometry and TUNEL assay were used to measure Hep G2 cell apoptosis. Western blotting and quantitative reverse transcription-polymerase chain reaction methods were used to determine the protein and messenger RNA levels of ER stress and apoptosis related genes' expression, respectively. Tissue microarray construction from patients was verified by immunohistochemical analysis.RESULTS In the present study, we first identified that melatoninselectively blocked activating transcription factor 6(ATF-6) and then inhibited cyclooxygenase-2 (COX-2) expression, leading to enhanced liver cancer cell apoptosis under ER stress condition. Dramatically increased CCAAT-enhancer-binding protein homologous protein level, suppressed COX-2 and decreased Bcl-2/Bax ratio by melatonin or ATF-6 si RNA contributed the enhanced Hep G2 cell apoptosis under tunicamycin (an ER stress inducer) stimulation. In clinical hepatocellular carcinoma patients, the close relationship between ATF-6 and COX-2 was further confirmed.CONCLUSION These findings indicate that melatonin as a novel selective ATF-6 inhibitor can sensitize human hepatoma cells to ER stress inducing apoptosis.

关键词： melatonin Endoplasmic 蜂窝胃应力激活抄写因素 6 Cyclooxygenase-2 Hepatocellular 癌

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melatonin Alleviates Acute Gouty Inflammation In Vivo and In Vitro

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Current Medical Science 2021年第4期41卷 757-763页

作者： Wen-ze XIAO Li ZHAO Lin CAO Xiao-xia ZHU He-jian ZOU Department of Rheumatology and Immunology Huashan Hospital Affiliated to Fudan UniversityShanghai 200040China Department of Rheumatology and Immunology Fudan University Pudong Medical CenterShanghai 201300China

The aim of this study was to identify the effects of melatonin on acute gouty inflammation and to investigate the underlying mechanisms.We found significantly lower serum melatonin levels in gout patients in the acute phase than in those in the remission phase or in normal individuals.The mRNA expression of melatonin receptor 2(MT2)was also lower in gout patients than in normal individuals.To verify the in-vivo role of melatonin,a gouty arthritis model was established by intraarticular injection of monosodium urate(MSU,1 mg)crystals into the paws of C57BL/6 mice.Joint inflammation in the mouse model was evaluated by measuring the thickness of the right paw/left paw,and the inflammation index was determined by examining infiltrating neutrophils with haematoxylin and eosin(H&E)staining.melatonin was found to reduce both paw thickness and the inflammation index in the mouse model,and melatonin also reduced the mRNA levels of interleukin-1 beta(IL-1β),IL-6 and NLR family pyrin domain containing 3(NLRP3)inflammasome.To mimic gouty inflammation in vitro,mouse peritoneal macrophages were stimulated with lipopolysaccharides(LPS)plus MSU.melatonin was revealed to reduce IL-1βsecretion by stimulated macrophages.The mRNA expression levels of IL-1βand IL-6 were also inhibited by melatonin.Western blot analysis showed that the expression of NLRP3,caspase-1 and pro-IL-1βwas also inhibited by melatonin.In conclusion,our study demonstrated that melatonin alleviated gouty inflammation in vivo and in vitro,and the underlying mechanism may involve inhibiting the assembly of the NLRP3 inflammasome.

关键词： melatonin gout NLRP3 inflammasome monosodium urate

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