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回医艾灸通过 Fas/FasL 信号通路促进大鼠腰椎间盘突出症吸收和运动功能恢复。

Hui Medicine Moxibustion Promotes the Absorption of Lumbar Disc Herniation and the Recovery of Motor Function in Rats through Fas/FasL Signaling Pathway.

机构信息

Traditional Chinese Medicine and Traumatology, General Hospital of Ningxia Medical University, Yinchuan, 750004 Ningxia, China.

Key Laboratory of Modernization of Traditional Chinese Medicine, Ningxia Medical University, Yinchuan, 750004 Ningxia, China.

出版信息

Biomed Res Int. 2022 Jul 23;2022:9172405. doi: 10.1155/2022/9172405. eCollection 2022.

DOI:10.1155/2022/9172405
PMID:35915787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9338866/
Abstract

OBJECTIVES

To study the resorption of the herniated lumbar disc (RHLD) and its mechanism in the SD rats of lumbar intervertebral disc herniation treated with Hui medicine moxibustion (HMM).

METHODS

Forty SD rats were randomly divided into four groups, normal group, lumbar disc herniation (LDH) group, HMM group, and antagonist (HMM+Met12) group, with 10 rats in each group. The rat model of LDH was prepared with the method of lumbar epidural emplacement of the caudal intervertebral disc. In the HMM group and HMM+Met12 groups, 4 weeks after modeling, HMM therapy was performed in the lumbar spine for 3 months with 1 time per day and 20 min each time, the samples were collected 8 weeks after the treatment. The histological degeneration was observed through HE staining, and the neovascularization of intervertebral disc tissues was detected by the expression of CD34 and vascular endothelial growth factor (VEGF). The apoptosis of nucleus pulpous cells was detected by TUNEL assay, and the activity of caspase-3, -8, and -9 and extracellular matrix enzymes was detected by western blotting.

RESULTS

HMM treatment significantly improved the behavioral ability of rats with LDH surgery. The morphological structure was obviously destroyed in the LDH group, but disc structure was significantly repaired in the HMM group, and mild structure alterations were observed in the HMM+Met12 group. Higher levels of CD34 and VEGF were detected in the HMM group indicating that neovascularization is formed. The expression level of FasL was significantly increased in the HMM group. The protein expression levels of cleaved-caspase-3, cleaved-caspase-8, and cleaved-caspase-9 in nucleus pulposus (NP) tissues were also elevated when treated with HMM, and the TUNEL staining showed the same results. The protein expression levels of matrix metalloproteinases- (MMP-) 1, MMP-2, MMP-3, MMP-13, and ADAMTS-4 were markedly promoted in the HMM group. Met12, a small peptide antagonist of FasL, significantly reduced the effects of HMM.

CONCLUSION

HMM can promote the formation of neovascularization of lumbar intervertebral disc, support the apoptosis of NP cells through Fas/FasL signaling, and regulate the degradation of extracellular matrix enzyme, which then accelerates the absorption of lumbar intervertebral disc herniation and the recovery of motor function in rats.

摘要

目的

研究回医艾灸疗法治疗腰椎间盘突出症大鼠模型(SD 大鼠)腰椎间盘突出症(RHLD)的吸收及其机制。

方法

40 只 SD 大鼠随机分为 4 组,正常组、腰椎间盘突出症(LDH)组、回医艾灸组(HMM)和拮抗剂(HMM+Met12)组,每组 10 只。采用腰椎硬膜外放置尾椎间椎间盘的方法制备 LDH 大鼠模型。在 HMM 组和 HMM+Met12 组中,建模后 4 周,每日 1 次,每次 20min,连续 3 个月进行 HMM 治疗,治疗后 8 周采集标本。通过 HE 染色观察组织学退变,通过 CD34 和血管内皮生长因子(VEGF)的表达检测椎间盘组织的新生血管形成。TUNEL 检测法检测核髓细胞凋亡,Western blot 检测 caspase-3、-8、-9 及细胞外基质酶的活性。

结果

HMM 治疗明显改善了 LDH 手术大鼠的行为能力。LDH 组形态结构明显破坏,HMM 组椎间盘结构明显修复,HMM+Met12 组结构改变轻微。HMM 组 CD34 和 VEGF 水平升高,提示新生血管形成。HMM 组 FasL 表达水平显著升高。HMM 处理后,核髓组织(NP)中 cleaved-caspase-3、cleaved-caspase-8 和 cleaved-caspase-9 的蛋白表达水平升高,TUNEL 染色也得到相同结果。HMM 组基质金属蛋白酶-(MMP-)1、MMP-2、MMP-3、MMP-13 和 ADAMTS-4 的蛋白表达水平显著升高。FasL 的小肽拮抗剂 Met12 显著降低了 HMM 的作用。

结论

HMM 可促进腰椎间盘新生血管形成,通过 Fas/FasL 信号支持 NP 细胞凋亡,调节细胞外基质酶降解,从而加速大鼠腰椎间盘突出症的吸收和运动功能的恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/aff9adfe9257/BMRI2022-9172405.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/23f9775cc100/BMRI2022-9172405.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/5e80982559fd/BMRI2022-9172405.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/4b3d6d1935d6/BMRI2022-9172405.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/aff9adfe9257/BMRI2022-9172405.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/23f9775cc100/BMRI2022-9172405.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/5e80982559fd/BMRI2022-9172405.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/4b3d6d1935d6/BMRI2022-9172405.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b4/9338866/aff9adfe9257/BMRI2022-9172405.004.jpg

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