title: Autophagy is involved in the effects of resveratrol on prevention of splenocyte apoptosis caused by oxidative stress in restrained mice.
abstract: METHODS
  Resveratrol, a powerful natural compound for human health, is widely reported for its immunity-related beneficial properties. However, few works have studied its effect mechanism on immunity. The present study was conducted to investigate the effects of resveratrol on splenic immunity in restraint stressed mice and the mechanism was further studied as autophagy induction.
  
  
  RESULTS
  Mice were administered with resveratrol for 7 days consecutively, fixed in restraint cages for 18 h, and recovered for 12 h after the last administration. Data showed that restraint led to spleen damages, including declined spleen index, decreased CD4(+) T-cell number, increased mitochondrial oxidative damage, and apoptosis of splenocytes. Resveratrol, vitamin C (antioxidant), and rapamycin (autophagy agonist) protected spleen functions. Meanwhile, rapamycin augmented the effects of resveratrol that were abolished by chloroquine (autophagy antagonists). Further studies showed that expressions of Beclin 1 and LC3β required in autophagy development were significantly upregulated by resveratrol but not by vitamin C.
  
  
  CONCLUSIONS
  This study demonstrated that resveratrol preserved splenic immunity of restraint stressed mice. It is meaningful to find that autophagy, apart from reactive oxygen species clearance, is included as a potential mechanism via which resveratrol ameliorated the state of oxidative stress and thus protected splenocytes in mice.
authors.affiliation: Pharmacy College, Jinan University, Guangzhou, PR China.
authors.forename: Wen-Jun
authors.initials: WJ
authors.lastname: Duan
authors.forename: Fang-Lan
authors.initials: FL
authors.lastname: Liu
authors.forename: Rong-Rong
authors.initials: RR
authors.lastname: He
authors.forename: Wei-Lin
authors.initials: WL
authors.lastname: Yuan
authors.forename: Yi-Fang
authors.initials: YF
authors.lastname: Li
authors.forename: Bun
authors.initials: B
authors.lastname: Tsoi
authors.forename: Wei-Wei
authors.initials: WW
authors.lastname: Su
authors.forename: Xin-Sheng
authors.initials: XS
authors.lastname: Yao
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kurihara
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001205:Ascorbic Acid / Q000494:pharmacology; D001343:Autophagy / Q000187:drug effects*; D000071186:Beclin-1; D020287:In Situ Nick-End Labeling; D008297:Male; D053078:Membrane Potential, Mitochondrial; D051379:Mice; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D000077185:Resveratrol; D020123:Sirolimus / Q000494:pharmacology; D013154:Spleen / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D013267:Stilbenes / Q000494:pharmacology*; D016176:T-Lymphocyte Subsets / Q000166:cytology; D015854:Up-Regulation
chemical_list: D000975:Antioxidants; D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; C115010:Becn1 protein, mouse; C480860:Map1lc3b protein, mouse; D008869:Microtubule-Associated Proteins; D017382:Reactive Oxygen Species; D013267:Stilbenes; D001205:Ascorbic Acid; D000077185:Resveratrol; D020123:Sirolimus
keywords: Autophagy; Oxidative stress; Restraint; Resveratrol; Splenocytes