VIP alleviates sepsis-induced cognitive dysfunction as the TLR-4/NF-κB signaling pathway is inhibited in the hippocampus of rats

被引:5
|
作者
Yang, Yujiao [1 ]
Yun, Debo [2 ]
Dong, Biqian [1 ]
Geng, Yuan [1 ]
Wan, Yong [1 ]
机构
[1] North Sichuan Med Coll, Dept Anesthesiol, Affiliated Hosp, 1 Maoyuan South Rd, Nanchong 637000, Sichuan, Peoples R China
[2] Nanchong Cent Hosp, Dept Neurosurg, Nanchong 637000, Sichuan, Peoples R China
关键词
VIP; TLR4; NF-kappa B; Cognitive impairment; Inflammation; Sepsis; VASOACTIVE-INTESTINAL-PEPTIDE; ACUTE LUNG INJURY; NEUROINFLAMMATION; ENCEPHALOPATHY; INFLAMMATION; MODEL;
D O I
10.1007/s10735-022-10068-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cognitive dysfunction caused by sepsis-associated encephalopathy (SAE) is still poorly understood. It is reported that vasoactive intestinal peptide (VIP) exerts its anti-inflammatory effects in multiple diseases, while its biological function in SAE remains unclear. We aimed to figure out whether VIP has influence on sepsis-induced neuroinflammation and cognitive dysfunction. To induce sepsis, rats were subjected to cecal ligation and puncture (CLP) operation. Morris water maze test and fear conditioning test were conducted to reveal cognitive dysfunctions. TUNEL assay was performed to evaluate apoptosis. We found out that the expression of VIP was downregulated in the hippocampus of septic rats. VIP was verified to attenuate sepsis-induced memory impairment following CLP. Additionally, we examined apoptosis and inflammation in rats' hippocampus. It is worth noting that VIP inhibited the apoptosis in the hippocampus and reduced the productions of proinflammatory cytokines TNF-alpha, IL-6 and IL-1 beta. Furthermore, our data confirmed that VIP was involved in regulating the TLR-4/NF-kappa B signaling. In conclusion, VIP inhibited neuroinflammation and cognitive impairment in hippocampus of septic rats through the TLR-4/NF-kappa B signaling pathway.
引用
收藏
页码:369 / 377
页数:9
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