Next Article in Journal
Protein-Phospholipid Interactions in Nonclassical Protein Secretion: Problem and Methods of Study
Previous Article in Journal
Covalent Coupling of Nanoparticles with Low-Density Functional Ligands to Surfaces via Click Chemistry
Int. J. Mol. Sci. 2013, 14(2), 3718-3733; doi:10.3390/ijms14023718
Article

Exercise Therapy Downregulates the Overexpression of TLR4, TLR2, MyD88 and NF-κB after Cerebral Ischemia in Rats

* ,
 and
Received: 28 September 2012; in revised form: 6 December 2012 / Accepted: 28 January 2013 / Published: 7 February 2013
View Full-Text   |   Download PDF [810 KB, uploaded 19 June 2014]   |   Browse Figures
Abstract: Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) are considered to mediate the inflammatory reaction of cerebral ischemia injury, and exercise can inhibit the activity of the Toll-like receptor signaling pathway in the peripheral blood of humans. Although physical exercise has been demonstrated to be neuroprotective in both clinical and laboratory settings, the underlying mechanism remains unclear. To clarify this critical issue, this study investigated the effects of treadmill training on the recovery of neurological function and the expression of TLR2 and TLR4 and their main downstream targets, nuclear factor-kappaB (NF-κB) and myeloid differentiation factor 88 (MyD88), in the ischemic rat brain after middle cerebral artery occlusion-reperfusion (MCAo/R). Rats were divided into seven groups: sham control without MCAo/R and five, nine and 16 days post-ischemic exercise or non-exercise. The neurological function and infarct volume were measured, and reverse transcription polymerase chain reaction (RT-PCR) and Western blotting were used to detect the expression of TLR2, TLR4, NF-κB and MyD88 in ischemic brain tissue. The results indicated that treadmill training promoted functional recovery and reduced the overexpression of TLR2, TLR4, NF-κB and MyD88 in rat brain tissue after ischemia, a finding that may have implications for understanding the mechanism of exercise therapy after brain ischemia and indicating new therapeutic strategies for the pharmacological modulation of TLR signaling.
Keywords: neuroprotection; cerebral ischemia; TLR2; TLR4; exercise; NF-κB; MyD88 neuroprotection; cerebral ischemia; TLR2; TLR4; exercise; NF-κB; MyD88
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Export to BibTeX |
EndNote


MDPI and ACS Style

Ma, Y.; He, M.; Qiang, L. Exercise Therapy Downregulates the Overexpression of TLR4, TLR2, MyD88 and NF-κB after Cerebral Ischemia in Rats. Int. J. Mol. Sci. 2013, 14, 3718-3733.

AMA Style

Ma Y, He M, Qiang L. Exercise Therapy Downregulates the Overexpression of TLR4, TLR2, MyD88 and NF-κB after Cerebral Ischemia in Rats. International Journal of Molecular Sciences. 2013; 14(2):3718-3733.

Chicago/Turabian Style

Ma, Yuewen; He, Man; Qiang, Lin. 2013. "Exercise Therapy Downregulates the Overexpression of TLR4, TLR2, MyD88 and NF-κB after Cerebral Ischemia in Rats." Int. J. Mol. Sci. 14, no. 2: 3718-3733.


Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert