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| GAO Chunpeng,ZHU Yu,ZHANG Peng.P38 mitogen-activated protein kinase inhibitor influence on the expression of MMPs and inflammatory factors in spontaneous resorption of ruptured herniated intervertebral discs[J].Chinese Journal of Spine and Spinal Cord,2017,(10):938-945. |
| P38 mitogen-activated protein kinase inhibitor influence on the expression of MMPs and inflammatory factors in spontaneous resorption of ruptured herniated intervertebral discs |
| Received:June 19, 2017 Revised:September 01, 2017 |
| English Keywords:Lumbar disc herniation Spontaneous resorption P38 mitogen-activated protein kinase TNF-α IL-1β Matrix metalloproteinases |
| Fund:国家自然科学基金资助项目（编号：81473691） |
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| English Abstract: |
| 【Abstract】 Objectives: To investigate the role of P38 mitogen-activated protein kinases(P38MAPK) signal phosphorylation in the lumbar intervertebral disc herniation spontaneous resorption. Methods: 40 Sprague Dawley(SD) rats were divided into experimental group(P38 MAPK inhibition) and control group(non-contained). The model of ruptured lumbar intervertebral disc herniation resorption was established on SD rat by putting two coccygeal intervertebral disc(IVDs) which were removed and injured prior into the subcutaneous space of the back where the L4-5 spinous and all vertebral plates were chewed and the dural sac was ruptured. Furthermore, experimental group was injected intraperitoneally by SB203580, and control group was injected by saline. At 1 and weeks 4 post-surgery, the rats were sacrificed, and the relocated discs were taken out for further testing. Morphological changes were examined by HE staining, and the mRNA and protein expressions of P38 mitogen-activated protein kinase(P38MAPK), phosphorylated p38 mitogen-activated protein kinase(P-p38MAPK), tumour necrosis factor-α(TNF-α), interleukin-1β(IL-1β), matrix metalloproteinase-3(MMP-3), matrix metalloproteinase-9(MMP-9) in intervertebral disc tissue were statistically determined by Real Time-PCR and Western-Blot. Results: In control group, the disc had a mass reduction of 4.15±1.84mg over the weekend, and 10.56±3.29mg decreased by 4 weeks(P<0.05). In experimental group, the reduction value of disc mass at 4 weeks and 1 week was respectively 1.11±3.05mg and 0.47±2.90mg, the difference was not statistically significant(P＞0.05). Under microscope, the tissue morphology of transplanted disc in control group showed obvious degeneration. The morphological degeneration of intervertebral disc tissue was not obvious in experimental group. Real Time PCR test results: over the week, the mRNA expression of TNF-α, p38MAPK, MMP-3 and MMP-9 of intervertebral discs in experimental group was significantly lower than that in control group(P<0.05). At 4 weeks, the mRNA expression of TNF-α, IL-1β, p38MAPK and MMP-3 in experimental group was significantly lower than that in control group(P<0.05). Western Blot test results: the protein expression of TNF-α, P38MAPK, P-p38MAPK and MMP-3 of intervertebral discs in experimental group was lower than that in control group at 4 weeks(P<0.05). In control group, the protein expression of TNF-α, IL-1β and P-p38MAPK of the intervertebral disc nucleus at 4 weeks was significantly higher than that at 1 weekend(P<0.05). The protein expressions of MMP-3, IL-1β, TNF-α were positively correlated with P38MAPK time-dependently in control group(0＜r＜1, P<0.05). Conclusions: The phosphorylation of P38MAPK signaling pathway can regulate inflammatory factor agglomeration, improve the expression of matrix metalloproteinase, and promote the resorption of nucleus pulposus. The P38MAPK-specific blocker can reduce the phosphorylation of P38MAPK and then reduce tthe expression levels of mRNA and protein of TNF-α, IL-1β, MMP-3 and MMP-9. The resorption effect was inhibited. |
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