PMID- 26431348
OWN - NLM
STAT- MEDLINE
DCOM- 20160822
LR  - 20211203
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 37
IP  - 4
DP  - 2015
TI  - Anti-Inflamm-Aging Effects of Long-Term Caloric Restriction via Overexpression of 
      SIGIRR to Inhibit NF-kappaB Signaling Pathway.
PG  - 1257-70
LID - 10.1159/000430248 [doi]
AB  - BACKGROUND: Chronic inflammation is thought to be a determinant of the aging rate 
      and longevity. Caloric restriction (CR) attenuates age-related increases in the 
      systemic levels of several pro-inflammatory mediators, but the anti-inflammatory 
      mechanisms of CR in the aging process remain unclear. METHODS: Fisher 344 rats in 
      a CR group were fed an amount of food corresponding to 60% of that fed to an ad 
      libitum-fed (AL) group for 8 months. Biochemical analyses and renal pathological 
      grading were used to analyze physiological status. Important signaling molecules 
      in the Toll-like receptor/nuclear factor kappa-light-chain-enhancer of activated 
      B cells (TLR/NF-kappaB) pathway were also analyzed by western blotting, 
      immunofluorescence and immunohistochemistry. RESULTS: 1) Compared with AL 
      feeding, CR decreased aging-mediated increases in both biochemical marker levels 
      and renal pathological grading. 2) Single immunoglobulin IL-1 (IL-1)-related 
      receptor (SIGIRR) expression decreased with increasing age, but CR led to 
      overexpression. 3) The expression of TLR4 was significantly higher in the CR 
      group than in the AL group. 4) SIGIRR overexpression decreased the expression of 
      the adaptor molecules myeloid differentiation factor 88 (MyD88), IL-1 
      receptor-associated kinase 4 (IRAK4) and tumor necrosis factor 
      receptor-associated factor 6 (TRAF6). 5) The levels of the inflammatory markers 
      phospho-IkappaBalpha and phospho-NF-kappaB p65 decreased in the CR group. CONCLUSIONS: The 
      inflammatory response might be alleviated by SIGIRR via blockade of the 
      TLR4/NF-kappaB signaling pathway. Therefore, CR can decrease inflammation via SIGIRR 
      overexpression, and SIGIRR might be a new target to delay aging.
CI  - (c) 2015 S. Karger AG, Basel.
FAU - Xu, Xiao-meng
AU  - Xu XM
FAU - Ning, Yi-Chun
AU  - Ning YC
FAU - Wang, Wen-juan
AU  - Wang WJ
FAU - Liu, Jie-qiong
AU  - Liu JQ
FAU - Bai, Xue-yuan
AU  - Bai XY
FAU - Sun, Xue-feng
AU  - Sun XF
FAU - Cai, Guang-yan
AU  - Cai GY
FAU - Chen, Xiang-mei
AU  - Chen XM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151005
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (TNF Receptor-Associated Factor 6)
RN  - 0 (Toll-Like Receptor 4)
RN  - EC 2.7.11.1 (IRAK4 protein, rat)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
MH  - *Aging
MH  - Animals
MH  - *Caloric Restriction
MH  - *Inflammation
MH  - Kidney/metabolism/pathology
MH  - Myeloid Differentiation Factor 88/metabolism
MH  - NF-kappa B/*metabolism
MH  - Protein Serine-Threonine Kinases/metabolism
MH  - Rats
MH  - Rats, Inbred F344
MH  - Receptors, Interleukin-1/genetics/*metabolism
MH  - Signal Transduction
MH  - TNF Receptor-Associated Factor 6/metabolism
MH  - Toll-Like Receptor 4/metabolism
EDAT- 2015/10/03 06:00
MHDA- 2016/08/23 06:00
CRDT- 2015/10/03 06:00
PHST- 2015/09/02 00:00 [accepted]
PHST- 2015/10/03 06:00 [entrez]
PHST- 2015/10/03 06:00 [pubmed]
PHST- 2016/08/23 06:00 [medline]
AID - 000430248 [pii]
AID - 10.1159/000430248 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2015;37(4):1257-70. doi: 10.1159/000430248. Epub 2015 Oct 
      5.