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Effect of allicin on cognitive dysfunction induced by propofol anesthesia in aged rats
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DOI   10.11656/j.issn.1672-1519.2022.04.23
Key Words   alicin;propofol;cognitive function;hippocampus;oxidative stress;inflammation
Author NameAffiliationE-mail
WEI Hongfang Handan Central Hospital, Handan 056000, China  
WANG Fei Handan Central Hospital, Handan 056000, China  
YANG Xiaobin Handan Central Hospital, Handan 056000, China  
YUAN Jinge Handan Central Hospital, Handan 056000, China  
WANG Rui Handan Central Hospital, Handan 056000, China  
LI Fei Handan Central Hospital, Handan 056000, China  
CHEN Yongxue Handan Central Hospital, Handan 056000, China yx20050618@163.com 
Abstract
    [Objective] To investigate the effect of allicin on the cognitive dysfunction induced by propofol anesthesia in aged rats and its mechanism.[Methods] The 120 twenty-months old SD rats were randomly divided into normal control group,model group,piracetam group (500 mg/kg) and allicin low,medium,high dose groups (5,10,20 mg/kg). Except for normal control group,all the other groups were given propofol at 100 mg/kg for anesthesia by intraperitoneal injection,and the drugs were given for 7 days in each group after modeling (the rats in normal control group and model group were given normal saline). The cognitive function of the rats in each group were evaluated by Morris water maze experiment,the pathological damage of hippocampal CA1 area neurons was detected by HE staining and the neuronal apoptosis was observed by TUNEL staining. The activity of superoxide dismutase (SOD),catalase (CAT) and the content of malondialdehyde (MDA) in lung tissue were detected by biochemical analysis method. The content of inflammatory cytokines including tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β),interleukin-6 (IL-6) were detected by ELISA method. The expression of nuclear factor E2 correlation factor 2 (Nrf2),Heme oxygenase-1 (HO-1),nuclear factor-κB (NF-κB) were determined by Western blot.[Results] Compared with model group,the escape latency of the rats in piracetam group and allicin medium,high dose groups were shorter and the number of crossing platforms was increased (P<0.05 or P<0.01). The neuronal pathology in hippocampal CA1 area improved significantly,the number of neuronal apoptosis was significantly reduced,and the apoptosis index (AI) was significantly reduced (P<0.05 or P<0.01). The activity of SOD,CAT were increased and the content of MDA,TNF-α,IL-1β,IL-6 were decreased(P<0.01). The expression of Nrf2,HO-1 were up-regulated and the NF-κB was down-regulated (P<0.01). Compared with piracetam group,the escape latency of the rats in allicin high dose groups was shorter and the number of crossing platforms was increased (P<0.05). The AI was significantly reduced (P<0.01). The activity of SOD was increased and the content of MDA,TNF-α were decreased(P<0.05 or P<0.01). The expression of Nrf2, HO-1 were up-regulated and the NF-κB was down-regulated (P<0.05 or P<0.01).[Conclusion] Allicin can improve the cognitive dysfunction induced by propofol anesthesia in aged rats,which mechanism may be related to activating the Nrf2/HO-1 pathway and inhibiting the expression of NF-κB protein,and then inhibiting neuronal apoptosis,oxidation,inflammatory in hippocampal CA1 area.

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