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热量限制减轻弗氏完全佐剂诱导的炎性疼痛，提高β-羟基丁酸表达并恢复脊髓自噬通量。

Caloric Restriction Alleviates CFA-Induced Inflammatory Pain Elevating β-Hydroxybutyric Acid Expression and Restoring Autophagic Flux in the Spinal Cord.

作者信息

Liu Chang, Zheng Xiaoting, Liu Lifang, Hu Yun, Zhu Qianyun, Zhang Jiawei, Wang Huan, Gu Er-Wei, Yang Zhilai, Xu Guanghong

机构信息

Department of Anesthesiology, First Affiliated Hospital, Anhui Medical University, Hefei, China.

Key Laboratory of Anesthesia and Perioperative Medicine of Anhui Higher Education Institutes, Hefei, China.

出版信息

Front Neurosci. 2022 Apr 28;16:828278. doi: 10.3389/fnins.2022.828278. eCollection 2022.

DOI:10.3389/fnins.2022.828278
PMID:35573301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9096081/
Abstract

Inflammatory pain is the most common type of pain encountered in clinical practice; however, the currently available treatments are limited by insufficient efficacy and side effects. Therefore, new methods to relieve inflammatory pain targeting new mechanisms are urgently needed. Preclinical investigations have shown that CR (calorie restriction) exerts analgesic effects in neuropathic and cancer pain; however, the effect of CR on chronic inflammatory pain remains unknown. During calorie restriction, autophagy, a lysosome-dependent degradation process, can be activated to support cell survival. In the present study, we investigated the analgesic effects of CR on complete Freund's adjuvant (CFA)-induced inflammatory pain. The accumulation of LC3-II and p62 showed impaired autophagic flux in the ipsilateral spinal cord of mice with CFA-induced inflammatory pain. CR alleviated mechanical allodynia and thermal hyperalgesia and reduced paw edema and pro-inflammatory factors following CFA administration. CR exerted an analgesic effect by restoring autophagic flux in the spinal cord. Regarding the mechanisms underlying the analgesic effects of CR, β-hydroxybutyric acid (BHB) was studied. CR increased BHB levels in the ipsilateral spinal cord. Furthermore, exogenous BHB administration exerted an analgesic effect by restoring autophagic flux in the spinal cords of CFA-induced inflammatory pain mice. Taken together, these results illustrated that CR relieved inflammatory pain by restoring autophagic flux in the spinal cord, while BHB controlled the benefits of CR, suggesting that CR or BHB might be a promising treatment for inflammatory pain.

摘要

炎性疼痛是临床实践中最常见的疼痛类型；然而，目前可用的治疗方法受到疗效不足和副作用的限制。因此，迫切需要针对新机制缓解炎性疼痛的新方法。临床前研究表明，热量限制（CR）对神经性疼痛和癌痛具有镇痛作用；然而，CR对慢性炎性疼痛的影响尚不清楚。在热量限制期间，自噬（一种溶酶体依赖性降解过程）可被激活以支持细胞存活。在本研究中，我们研究了CR对完全弗氏佐剂（CFA）诱导的炎性疼痛的镇痛作用。LC3-II和p62的积累表明CFA诱导的炎性疼痛小鼠同侧脊髓中的自噬流受损。CR减轻了机械性异常性疼痛和热痛觉过敏，并减少了CFA给药后的爪部水肿和促炎因子。CR通过恢复脊髓中的自噬流发挥镇痛作用。关于CR镇痛作用的潜在机制，我们研究了β-羟基丁酸（BHB）。CR增加了同侧脊髓中的BHB水平。此外，外源性给予BHB通过恢复CFA诱导的炎性疼痛小鼠脊髓中的自噬流发挥镇痛作用。综上所述，这些结果表明CR通过恢复脊髓中的自噬流缓解炎性疼痛，而BHB介导了CR的益处，这表明CR或BHB可能是炎性疼痛的一种有前景的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1830/9096081/53e80cd22343/fnins-16-828278-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1830/9096081/16e02c890603/fnins-16-828278-g002.jpg
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