光生物调节疗法（904nm）对链脲佐菌素诱导的糖尿病神经病变的抗痛觉过敏作用提示 MAPK 通路和钙动力学的调节。

Anti-hyperalgesic effects of photobiomodulation therapy (904 nm) on streptozotocin-induced diabetic neuropathy imply MAPK pathway and calcium dynamics modulation.

机构信息

Department of Structural and Functional Biology, Institute of Biology, University of Campinas (UNICAMP), Carl von Linnaeus n/n, Cidade Universitária Zeferino Vaz, Campinas, SP, 13083-864, Brazil.

出版信息

Sci Rep. 2022 Oct 6;12(1):16730. doi: 10.1038/s41598-022-19947-2.

DOI:10.1038/s41598-022-19947-2

PMID:36202956

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9537322/

Abstract

Several recent studies have established the efficacy of photobiomodulation therapy (PBMT) in painful clinical conditions. Diabetic neuropathy (DN) can be related to activating mitogen-activated protein kinases (MAPK), such as p38, in the peripheral nerve. MAPK pathway is activated in response to extracellular stimuli, including interleukins TNF-α and IL-1β. We verified the pain relief potential of PBMT in streptozotocin (STZ)-induced diabetic neuropathic rats and its influence on the MAPK pathway regulation and calcium (Ca) dynamics. We then observed that PBMT applied to the L4-L5 dorsal root ganglion (DRG) region reduced the intensity of hyperalgesia, decreased TNF-α and IL-1β levels, and p38-MAPK mRNA expression in DRG of diabetic neuropathic rats. DN induced the activation of phosphorylated p38 (p-38) MAPK co-localized with TRPV1 neurons; PBMT partially prevented p-38 activation. DN was related to an increase of p38-MAPK expression due to proinflammatory interleukins, and the PBMT (904 nm) treatment counteracted this condition. Also, the sensitization of DRG neurons by the hyperglycemic condition demonstrated during the Ca dynamics was reduced by PBMT, contributing to its anti-hyperalgesic effects.

摘要

最近的几项研究已经证实了光生物调节疗法（PBMT）在治疗疼痛性临床病症方面的疗效。糖尿病性周围神经病变（DN）可能与外周神经中丝裂原活化蛋白激酶（MAPK），如 p38 的激活有关。MAPK 通路在受到细胞外刺激（包括 TNF-α 和 IL-1β 等细胞因子）时被激活。我们验证了 PBMT 在链脲佐菌素（STZ）诱导的糖尿病性神经病变大鼠中的镇痛潜力，以及其对 MAPK 通路调节和钙（Ca）动力学的影响。结果发现，应用于 L4-L5 背根神经节（DRG）区域的 PBMT 可减轻痛觉过敏的强度，降低 DRG 中 TNF-α 和 IL-1β 的水平，以及糖尿病性神经病变大鼠的 p38-MAPK mRNA 表达。DN 诱导磷酸化 p38（p-38）MAPK 与 TRPV1 神经元共定位的激活；PBMT 部分阻止了 p-38 的激活。DN 与促炎细胞因子有关，p38-MAPK 表达增加，而 PBMT（904nm）治疗则抑制了这种情况。此外，高血糖条件下 DRG 神经元的敏化作用通过 PBMT 降低，这有助于其抗痛觉过敏作用。