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Effect of relaxation-dependent adhesion on pre-sliding response of cartilage.

ABSTRACT: Possible links between adhesive properties and the pre-sliding (static) friction response of cartilage are not fully understood in the literature. The aims of this study are to investigate the relation between adhesion and relaxation time in articular cartilage, and the effect of relaxation-dependent adhesion on the pre-sliding response of cartilage. Adhesion tests were performed to evaluate the work of adhesion of cartilage at different relaxation times. Friction tests were conducted to identify the pre-sliding friction response of cartilage at relaxation times corresponding to adhesion tests. The pre-sliding friction response of cartilage was systematically linked to the work of adhesion and contact conditions by a slip-based failure model. It was found that the work of adhesion increases with relaxation time. Also, the work of adhesion is linearly correlated to the resistance to slip-based failure. In addition, as the work of adhesion increases, the adhered (stick) area at the moment of failure increases, and the propagation rate of the annular slip (crack) area towards its centre increases. These findings offer a mechanistic explanation of the pre-sliding friction behaviour and stick-slip response of soft hydrated interfaces such as articular cartilage and hydrogels. In addition, the linear correlation between adhesion and threshold to slip-based failure enables estimation of the adhesive strength of such interfaces directly from the pre-sliding friction response (e.g. shear wave elastography).

SUBMITTER: Han G

PROVIDER: S-EPMC5990745 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature

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Effect of relaxation-dependent adhesion on pre-sliding response of cartilage.

Han Guebum G Eriten Melih M

Royal Society open science 20180523 5

Possible links between adhesive properties and the pre-sliding (static) friction response of cartilage are not fully understood in the literature. The aims of this study are to investigate the relation between adhesion and relaxation time in articular cartilage, and the effect of relaxation-dependent adhesion on the pre-sliding response of cartilage. Adhesion tests were performed to evaluate the work of adhesion of cartilage at different relaxation times. Friction tests were conducted to identif ...[more]

PMID: 29892390

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Project description:Tetrahydropalmatine (THP) is an active natural alkaloid isolated from Corydalis yanhusuo W.T. Wang which has been widely used for treating pain and cardiovascular disease in traditional Chinese medicine. Previous studies suggested THP have various pharmacological effects in neural and cardio tissue while the vascular reactivity of THP was not fully established. The present study found that THP relaxed rat aorta which contracted by phenylephrine (Phe), KCl, and U46619. The vascular relaxation effect of THP was partially attenuated by PI3K inhibitor wortmannin, Akt inhibitor IV, endothelial nitric oxide synthetase (eNOS) inhibitor L-NAME, guanylate cyclase inhibitors and the mechanical removal of endothelium. Also, the eNOS substrate L-arginine reversed the inhibition effect of L-NAME on THP-induced vascular relaxation. THP also induced intracellular NO production in human umbilical vein endothelial cells. However, Pre-incubation with β-adrenergic receptor blocker propranolol, angiotensin II receptor 1 (AT1) inhibitor losartan, angiotensin II receptor 2 (AT1) inhibitor PD123319 or angiotensin converting enzyme inhibitor enalapril enhanced the vascular relaxation effect of THP. THP did not affect the angiotensin II induced vascular contraction. Cyclooxygenase-2 (COX2) inhibitor indomethacin did not affect the vascular relaxation effect of THP. Furthermore, pre-treatment THP attenuated KCl and Phe induced rat aorta contraction in standard Krebs solution. In Ca2+ free Krebs solution, THP inhibited the Ca2+ induced vascular contraction under KCl or Phe stress and reduced KCl stressed Ca2+ influx in rat vascular smooth muscle cells. THP also inhibited intracellular Ca2+ release induced vascular contraction by blocking Ryr or IP3 receptors. In addition, the voltage-dependent K+ channel (Kv) blocker 4-aminopyridine, ATP-sensitive K+ channel (KATP) blocker glibenclamide and inward rectifying K+ channel blocker BaCl2 attenuated THP induced vascular relaxation regardless of the Ca2+-activated K+ channel (KCa) blocker tetraethylammonium. Thus, we could conclude that THP relaxed rat aorta in an endothelium-dependent and independent manner. The underlying mechanism of THP relaxing rat aorta involved PI3K/Akt/eNOS/NO/cGMP signaling path-way, Ca2+ channels and K+ channels rather than COX2, β-adrenergic receptor and renin-angiotensin system (RAS). These findings indicated that THP might be a potent treatment of diseases with vascular dysfunction like hypertension.

Dataset Information

Effect of relaxation-dependent adhesion on pre-sliding response of cartilage.

Publications

Effect of relaxation-dependent adhesion on pre-sliding response of cartilage.

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