Decreased serum level of HMGB1 and MyD88 during human aging progress in healthy individuals
Aims Previous studies have suggested that high mobility group box-1 protein (HMGB1) binds to the toll-like receptor 4 (TLR4) signaling mediates the progression of various inflammatory diseases. But the roles of HMGB1 and TLR4 in aging remain poorly unknown. In this study, we aimed to investigate the...
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Published in | Aging clinical and experimental research Vol. 28; no. 2; pp. 175 - 180 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Cham
Springer International Publishing
01.04.2016
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Aims
Previous studies have suggested that high mobility group box-1 protein (HMGB1) binds to the toll-like receptor 4 (TLR4) signaling mediates the progression of various inflammatory diseases. But the roles of HMGB1 and TLR4 in aging remain poorly unknown. In this study, we aimed to investigate the serum levels of HMGB1 and myeloid differentiation factor 88 (MyD88), which is one of TLR4’s intracellular adaptor proteins during human aging process and their relevance with cathepsin B (CTSB).
Methods
This research was conducted using the blood samples provided by healthy people (
n
= 90, 63 men and 27 women). Subjects were subdivided into groups with respect to age: young (about 25 years old,
n
= 30), middle age (about 40 years old,
n
= 30), and aged (above 65 years old,
n
= 30). Altered serum levels of HMGB1, MyD88 and CTSB were measured using an enzyme-linked immunosorbent assay.
Results
The serum levels of HMGB1 and MyD88 were significantly decreased in the aged group compared with those in the young group. Linear regression analysis showed that HMGB1 and MyD88 positively correlated with CTSB among the whole healthy people. A negative correlation was determined between MyD88 and age.
Conclusions
The serum levels of HMGB1 and MyD88
s
ignificantly decreased with age. MyD88, but not HMGB1, was negatively correlated with age. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1720-8319 1594-0667 1720-8319 |
DOI: | 10.1007/s40520-015-0402-8 |