PMID- 36653007 OWN - NLM STAT- MEDLINE DCOM- 20230120 LR - 20230120 IS - 1003-0034 (Print) IS - 1003-0034 (Linking) VI - 36 IP - 1 DP - 2023 Jan 25 TI - [Analysis of the effect of midazolam on pain in a rat model of lumbar disc herniation based on the p38 MAPK signaling pathway]. PG - 55-60 LID - 10.12200/j.issn.1003-0034.2023.01.010 [doi] AB - OBJECTIVE: To investigate the effect of midazolam on pain in lumbar disc herniation model rats based on p38 MAPK signaling pathway. METHODS: Fifty SPF-grade Sprague-Dawley healthy rats, half male and half female, were selected and randomly divided into normal group, model group, and low-dose, medium-dose, high-dose groups. Model group and low-dose, medium-dose, high-dose groups were initially modeled for lumbar disc herniation. Intraperitoneal injection of saline was performed in rats of normal and model groups; and in the low-dose, medium-dose, and high-dose groups, intraperitoneal injection of midazolam was performed with doses of 30, 60, and 90 mg/kg, respectively. Interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), 5-hydroxytryptamine (5-HT), beta-endorphin (beta-EP), substance P (SP), neuropeptide Y (NPY) were detected in the serum of rats by enzyme-linked immunoassay. The expression of p38 MAPK and matrix metalloproteinase-3(MMP-3) protein were detected by Western blot in the tissues of rats of each group. RESULTS: The levels of TNF-alpha, IL-1beta and beta-EP were higher and the level of 5-HT was lower in the model group than in the normal group(P<0.05);the levels of TNF-alpha, IL-1beta and beta-EP were lower and the level of 5-HT was higher in the low-dose, medium-dose and high-dose groups than in the model group(P<0.05). The levels of SP and NPY increased in the model group compared with the normal group (P<0.05) and the levels of SP and NPY decreased in the low-dose, medium-dose and high-dose groups compared with the model group (P<0.05). The expression of p38 MAPK and MMP-3 increased in the model group compared with the normal group (P<0.05); the expression of p38 MAPK and MMP-3 decreased in the low-dose, medium-dose and high-dose compared with the model group(P<0.05). CONCLUSION: Midazolam may ameliorate the immune inflammatory response in rats with a model of lumbar disc herniation, possibly regulated through the p38MAPK signaling pathway. FAU - Liu, Jian AU - Liu J AD - Department of Anesthesiology, Kailuan General Hospital Zhaogezhuang Hospital, Guzhi 063101, Hebei, China. FAU - Ye, Yu-Jun AU - Ye YJ AD - Department of Anesthesiology, Tangshan Hospital of Traditional Chinese Medicine, Tangshan 063000, Hebei, China. FAU - Liu, Shu-Min AU - Liu SM AD - Department of Anesthesiology, Kailuan General Hospital Zhaogezhuang Hospital, Guzhi 063101, Hebei, China. FAU - Liu, Shuang AU - Liu S AD - Department of Surgery, Kailuan General Hospital Zhaogezhuang Hospital, Guzhi 063101, Hebei, China. LA - chi PT - English Abstract PT - Journal Article PL - China TA - Zhongguo Gu Shang JT - Zhongguo gu shang = China journal of orthopaedics and traumatology JID - 9815790 RN - EC 3.4.24.17 (Matrix Metalloproteinase 3) RN - R60L0SM5BC (Midazolam) RN - 0 (Tumor Necrosis Factor-alpha) RN - 333DO1RDJY (Serotonin) RN - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) SB - IM MH - Rats MH - Male MH - Female MH - Animals MH - *Intervertebral Disc Displacement/drug therapy/pathology MH - Rats, Sprague-Dawley MH - Matrix Metalloproteinase 3/metabolism MH - Midazolam MH - Tumor Necrosis Factor-alpha/metabolism MH - Serotonin/metabolism MH - MAP Kinase Signaling System/physiology MH - Pain MH - p38 Mitogen-Activated Protein Kinases/metabolism OTO - NOTNLM OT - Immunity OT - Inflammation OT - Intervertebral disk displacement OT - Lumbar vertebrae OT - Pain OT - p38MAPK signaling pathway EDAT- 2023/01/19 06:00 MHDA- 2023/01/21 06:00 CRDT- 2023/01/18 19:52 PHST- 2023/01/18 19:52 [entrez] PHST- 2023/01/19 06:00 [pubmed] PHST- 2023/01/21 06:00 [medline] AID - 10.12200/j.issn.1003-0034.2023.01.010 [doi] PST - ppublish SO - Zhongguo Gu Shang. 2023 Jan 25;36(1):55-60. doi: 10.12200/j.issn.1003-0034.2023.01.010.