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汤剂通过调节背根神经节中的Sema3G蛋白缓解慢性炎性疼痛的作用机制。

Mechanism of action of decoction in relieving chronic inflammatory pain via Sema3G protein regulation in the dorsal root ganglion.

作者信息

Lin Rong, Gu Jun-Gang, Wang Zhi-Fu, Zeng Xiao-Xia, Xiao Hong-Wei, Chen Jin-Cheng, He Jian

机构信息

College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, China.

Affiliated Rehabilitation Hospital, Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China.

出版信息

Heliyon. 2023 Dec 12;10(1):e23617. doi: 10.1016/j.heliyon.2023.e23617. eCollection 2024 Jan 15.

DOI:10.1016/j.heliyon.2023.e23617
PMID:38192809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10772129/
Abstract

OBJECTIVE

The purpose of this study was to analyze the impact of decoction (SGD) on proteins with significant changes in the dorsal root ganglion (DRG) in rats and to explore the role of the Semaphorin 3G (Sema3G) protein in the DRG and its downstream factors, interleukin-6 (IL-6) and CC-motif chemokine ligand 2(CCL2), in the treatment of chronic inflammatory pain (CIP).

METHODS

We created a CIP rat model using 100 μL of complete Freund's adjuvant (CFA) that was injected into the left posterior plantar of rats. Then, we administered SGD intragastrically. We tested the animals for behavioral changes and protein expression levels in DRG pre- and post-drug intervention.

RESULTS

Rats in the SGD group showed significantly increased paw withdrawal threshold (PWT), paw withdrawal latency (PWL), and relative expression levels of the Sema3G protein in the DRG (all  < 0.05), while the relative mRNA expression levels of IL-6 and CCL2 in the DRG of the rats were significantly decreased ( < 0.05) when compared with the model group.

CONCLUSION

In this study, we found that decoction was effective in improving the PWT and PWL of rats with CIP. It reduced CIP by upregulating the expression of Sema3G in the DRG and inhibiting the relative mRNA expression levels of IL-6 and CCL2.

摘要

目的

本研究旨在分析疏骨丹（SGD）对大鼠背根神经节（DRG）中发生显著变化的蛋白质的影响，并探讨信号素3G（Sema3G）蛋白在DRG及其下游因子白细胞介素-6（IL-6）和CC基序趋化因子配体2（CCL2）在慢性炎性疼痛（CIP）治疗中的作用。

方法

我们使用100μL完全弗氏佐剂（CFA）给大鼠左后足底注射，建立CIP大鼠模型。然后，对大鼠进行灌胃给予SGD。我们在药物干预前后测试动物的行为变化和DRG中的蛋白质表达水平。

结果

SGD组大鼠的爪退缩阈值（PWT）、爪退缩潜伏期（PWL）以及DRG中Sema3G蛋白的相对表达水平均显著升高（均P<0.05），而与模型组相比，大鼠DRG中IL-6和CCL2的相对mRNA表达水平显著降低（P<0.05）。

结论

在本研究中，我们发现疏骨丹能有效改善CIP大鼠的PWT和PWL。它通过上调DRG中Sema3G的表达并抑制IL-6和CCL2的相对mRNA表达水平来减轻CIP。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/47c66b76242f/mmcfigs4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/a6badfae76b1/mmcfigs1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/4f31f807fe7d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/bee8d0276b58/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/e5d3517b123f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/577d15c1fcbb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/d6e4576f71e3/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/cb643c8edacf/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/c3f384ae8e68/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/2b9a64635c14/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/cb17e9707edc/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/bd0447ecaef5/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/ed767b62bebc/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/2d8cdd35fe8b/gr12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/ccc06ceeda62/gr13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/149f3d95ba6c/gr14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/a6badfae76b1/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/959f8760e85f/mmcfigs2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d7/10772129/47c66b76242f/mmcfigs4.jpg

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Shaoyao-Gancao Decoction Relieves Visceral Hyperalgesia in TNBS-Induced Postinflammatory Irritable Bowel Syndrome via Inactivating Transient Receptor Potential Vanilloid Type 1 and Reducing Serotonin Synthesis.芍药甘草汤通过失活瞬时受体电位香草酸亚型1和减少5-羟色胺合成减轻TNBS诱导的炎症后肠易激综合征中的内脏痛觉过敏。
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