Anti-inflammatory Effect of Heat-sensitive Moxibustion via the NF-κB Signaling Pathway on Cerebral Ischemia/Reperfusion Injury in Rats

• 作者: Aijiao Xiaoa Lin He Mingren Chen Xin OuYang Yisheng Xiaoa
• 来源期刊: 医学科学进展杂志(英文)
• 学科: 医学
• 关键词: Auspended MOXIBUSTION HEAT-SENSITIVE MOXIBUSTION Middle CEREBRAL artery occlusion CEREBRAL ISCHEMIA/REPERFUSION injury Tail temperature Tail-flick LATENCY INFARCT volume Inflammatory cells CD11b ICAM-1 NF-κB p65 p-IKKα/β Traditional Chinese Medicine
• 年，卷（期）: yxkxjzzzyw_2018,（3）
• 页码范围: 67-79
• 页数: 13页
• 分类号: R363

摘要

Ischemic stroke is universally acknowledged as a common cause of long-term disability or even death. Suspended moxibustion, an indirect form of moxibustion, is when moxibustion is placed superficially over the skin without being in contact with it. Some researchers have used this method to treat stroke patients, but strong evidence of its therapeutic effectiveness is lacking. However, the effect of traditional suspended moxibustion has recently been improved with the development of heat-sensitive suspended moxibustion. Our previous studies showed that moxibustion for 35 min provided a more effective treatment strategy than moxibustion for 15 min, and moxibustion by 35 min with tail temperature increase had a better outcome than that without, however, the mechanism underlying the effect is not clear. In this study, we treated the stroke rats with moxibustion by 35min and divided them into non-heat sensitive moxibustion(NHSM) group and heat sensitive moxibustion (HSM) group according to difference in the tail temperature increase, then we compared the effect and investigated the mechanisms between NHSM and HSM. We found that HSM significantly decreased tail-flick latency, increased neurological function score, decreased infarct volume, reduced inflammatory cells, decreased the expression of inflammatory factor ICAM-1 and reduced the expression of NF-κB p65 and p-IKKα/β in rats with focal cerebral ischemia/reperfusion injury. Our experimental findings revealed that HSM exerted its anti-inflammatory and neuroprotective effects from MCAO-induced injury by decreasing the expression of the NF-κB signaling pathway.