scholarly journals Morin Attenuates Interleukin-1 beta-Induced Inflammatory Response in Primary Rat Chondrocytes by Suppressing the Overproduction of Nitric Oxide and Matrix Metalloproteinases

2020 ◽  
Vol 82 (2) ◽  
Author(s):  
JING SHI ◽  
WEI YAO ◽  
SHILEI PANG
Keyword(s):  
Nitric Oxide ◽  
Matrix Metalloproteinases ◽  
Inflammatory Response ◽  
Interleukin 1 ◽  
Interleukin 1 Beta

scholarly journals Platelets inhibit the induction of nitric oxide synthesis by interleukin-1 beta in vascular smooth muscle cells

Blood ◽  
1994 ◽  
Vol 83 (7) ◽  
pp. 1831-1838 ◽  
Author(s):  
W Durante ◽  
VB Schini ◽  
MH Kroll ◽  
S Catovsky ◽  
T Scott-Burden ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Interleukin 1 ◽  
Muscle Cells ◽  
Interleukin 1 Beta ◽  
Functional Assays ◽  
Platelet Releasate

We have investigated the role of platelets in regulating the hemostatic and vasomotor properties of vascular smooth muscle. Experiments were performed to examine the effect of the releasate from activated platelets on the production of nitric oxide from interleukin-1 beta (IL- 1 beta)-treated cultured rat aortic smooth muscle cells. Treatment of vascular smooth muscle cells with IL-1 beta resulted in significant accumulation of nitrite in the culture media and in marked elevation of intracellular cyclic guanosine monophosphate (GMP) levels. The releasate from collagen-aggregated platelets blocked the IL-1 beta- mediated production of nitrite and the accumulation of cyclic GMP in smooth muscle cells in a platelet number-dependent manner. In functional assays, the perfusates from columns containing IL-1 beta- treated smooth muscle cells relaxed detector blood vessels without endothelium and the addition of IL-1 beta-treated smooth muscle cells to suspensions of platelets inhibited their thrombin-induced aggregation. The simultaneous treatment of smooth muscle cells with IL- 1 beta and the platelet releasate abolished both the vasorelaxing activities of the perfusates and the inhibition of platelet aggregation. Platelet releasates treated with a neutralizing antibody to platelet-derived growth factor (PDGF) failed to block IL-1 beta- induced nitric oxide production by the smooth muscle cells, as measured by both biochemical and functional assays. The platelet releasate from a patient with gray platelet syndrome likewise failed to block IL-1 beta-induced nitrite release by smooth muscle cells. These results demonstrate that platelets downregulate the production of nitric oxide by IL-1 beta-treated vascular smooth muscle cells through the release of PDGF. This effect may represent a novel mechanism by which platelets regulate vasomotor tone and thrombus formation at sites of vascular injury.

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