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Galectin-3抑制與神經(jīng)性疼痛周圍神經(jīng)損傷后衰減
Zhicong Ma1,2☯, Qi Han3☯, Xiaolei Wang3☯, Zisheng Ai4, Yongjun Zheng3*　

　
　　摘要
　　神經(jīng)性疼痛仍然是一個普遍和持久的臨床問題,因為它通常是不適應當前使用止痛劑。非常迫切需要開發(fā)出新的藥物來緩解神經(jīng)性疼痛。Galectin-3 (gal3)是一種多功能蛋白屬于汽車——bohydrate-ligand凝集素家族,由不同的細胞表達。新興的研究表明gal3誘導出促炎癥反應通過招募和激活lympho cytes,巨噬細胞和小膠質(zhì)細胞。在這項研究中,我們調(diào)查是否gal3抑制會抑制周圍神經(jīng)損傷后神經(jīng)炎癥和緩解神經(jīng)性疼痛。我們發(fā)現(xiàn)L5脊神經(jīng)結(jié)扎(SNL)增加的表達在背根神經(jīng)節(jié)gal3 mRNA和蛋白水平。鞘內(nèi)管理修改柑橘果膠(MCP), gal3抑制劑,減少gal3表達式在背根神經(jīng)節(jié)。

Galectin-3 Inhibition Is Associated with Neuropathic Pain Attenuation after Peripheral Nerve Injury
Zhicong Ma1,2☯, Qi Han3☯, Xiaolei Wang3☯, Zisheng Ai4, Yongjun Zheng3*
1 Department of Anesthesiology, The 2nd Hospital of Shanxi Medical University, Taiyuan, 030001, China,
2 Department of Anesthesiology, Xiangya Hospitalaffiliated to Central South University, Changsha 410008, China, 3 Department of Pain Management and Shanghai Key Laboratory of Clinical Geriatric Medicine, Huadong Hospital affiliated to Fudan University, No.221, West Yan'an Road, Shanghai, 200040, China,
4 Department of Preventive Medicine, College of Medicine, Tongji University, Shanghai 200092, China
☯ These authors contributed equally to this work.
* zhengyongjun1971@126.

Abstract
Neuropathic pain remains a prevalent and persistent clinical problem because it is often poorly responsive to the currently used analgesics. It is very urgent to develop novel drugs to alleviate neuropathic pain. Galectin-3 (gal3) is a multifunctional protein belonging to the car- bohydrate-ligand lectin family, which is expressed by different cells. Emerging studies showed that gal3 elicits a pro-inflammatory response by recruiting and activating lympho- cytes, macrophages and microglia. In the study we investigated whether gal3 inhibition could suppress neuroinflammation and alleviate neuropathic pain following peripheral nerve injury. We found that L5 spinal nerve ligation (SNL) increases the expression of gal3 in dorsal root ganglions at the mRNA and protein level. Intrathecal administration of modified citrus pectin(MCP), a gal3 inhibitor, reduces gal3 expression in dorsal root ganglions. MCP treatment also inhibits SNL-induced gal3 expression in primary rat microglia. SNL results in an increased activation of autophagy that contributes to microglial activation and subsequent inflammatory response. Intrathecal administration of MCP significantly suppresses SNL-induced autop- hagy activation. MCP also inhibits lipopolysaccharide (LPS)-induced autophagy in cultured microglia in vitro. MCP further decreases LPS-induced expression of proinflammatory media- tors including IL-1β, TNF-α and IL-6 by regulating autophagy. Intrathecal administration of MCP results in adecreased mechanical and cold hypersensitivity following SNL. These results demonstrated that gal3 inhibition is associated with the suppression of SNL-induced inflammatory process andneurophathic pain attenuation.