研究表明，利多卡因具有抗氧化应激、抗炎和神经保护作用。目前的研究调查了利多卡因对认知功能障碍大鼠认知功能的影响。总共 48 只大鼠被随机分为 4 组，每组 12 只大鼠：对照组； L(利多卡因)  D(d-半乳糖)组、d-半乳糖组(D组)；和D  L组。我们使用莫里斯水迷宫（MWM）和海马切片的病理变化评估认知功能。采用酶联免疫吸附法（ELIZA）检测大鼠血清丙二醛（MDA）和超氧化物歧化酶（SOD）水平，采用蛋白质免疫印迹（western blot）检测脑组织蛋白（塌陷反应介质蛋白-2）。 CRMP2]、磷酸化塌陷反应介导蛋白-2 [P-CRMP2]和β-淀粉样蛋白[Aβ])。MWM显示d-gal组(284.09 ± 20.46, 5.20 ± 0.793)表现差于L D组（265.37 ± 22.34、4.170 ±0.577；p = .000）和D  L组（254.72 ± 27.87、3.750；p = .000）的逃避潜伏期和平台穿越次数分别为。 L  D组（44.94 ± 2.92 pg/mL，6.22 ± 0.50 pg/mL，460.02 ± 8.26 nmol/mL）和D  L组（46.88 ± 2.63 pg/mL，5 .90 ± 0.38 pg/mL和465.6 ± 16.07 nmol/mL）的血清白介素-6、肿瘤坏死因子-α和MDA炎症水平显着低于d-gal组（57.79±3.96pg/mL、11.25±1.70pg/mL和564.9±15.90nmol/mL）毫升），分别。 L  D组(3.17±0.41μg/mL)和D  L组(3.08±0.09μg/mL)血清SOD炎症水平显着高于d-gal组(2.20±0.13μg/mL)(所有p = .000）。 L  D组（0.87 ± 0.04、0.57 ± 0.0、0.16 ± 0.02）和D  L组（0.82 ± 0.05、0.58）脑组织匀浆中CRMP2、P-CRMP2和Aβ的水平 ± 0.09，并且0.15±0.02）与d-gal组（0.67±0.03、0.96±0.040和0.29±0.05）有显着差异。利多卡因通过联合抗炎和抗氧化应激机制减轻认知功能障碍大鼠的认知障碍具有 CRMP2 抗磷酸化作用。© 2023 作者。约翰·威利出版的《免疫、炎症和疾病》

Studies have shown that lidocaine has antioxidative stress, anti-inflammatory, and nerve-protective effects. The current study investigated the effects of lidocaine on cognitive function in rats with cognitive dysfunction.A total of 48 rats were randomly assigned to four groups of 12 rats each: control group; L (lidocaine) + D (d-galactose) group, d-galactose group (D group); and D + L group. We assessed cognitive function using a Morris water maze (MWM) and pathologic changes of hippocampal sections. An enzyme-linked immunosorbent assay (ELIZA) was used to detect serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels in rats, and protein immunoblotting (western blot) was used to detect brain tissue proteins (collapsing response mediator protein-2 [CRMP2], phosphorylated-collapsing response mediator protein-2 [P-CRMP2], and β-amyloid protein [Aβ]).The MWM showed that the d-gal group (284.09 ± 20.46, 5.20 ± 0.793) performed worse than the L + D (265.37 ± 22.34, 4.170 ± 0.577; p = .000) and D + L groups (254.72 ± 27.87, 3.750; p = .000) in escape latency and number of platform crossings, respectively. The L + D group (44.94 ± 2.92 pg/mL, 6.22 ± 0.50 pg/mL, and 460.02 ± 8.26 nmol/mL) and D + L group (46.88 ± 2.63 pg/mL, 5.90 ± 0.38 pg/mL, and 465.6 ± 16.07 nmol/mL) had significantly lower serum inflammatory levels of interleukin-6, tumor necrosis factor-α, and MDA than the d-gal group (57.79 ± 3.96 pg/mL, 11.25 ± 1.70 pg/mL, and 564.9 ± 15.90 nmol/mL), respectively. The L + D group (3.17 ± 0.41 μg/mL) and D + L group (3.08 ± 0.09 μg/mL) had significantly higher serum inflammatory levels of SOD than the d-gal group (2.20 ± 0.13 μg/mL) (all p = .000). The levels of CRMP2, P-CRMP2, and Aβ in the brain tissue homogenates of the L + D group (0.87 ± 0.04, 0.57 ± 0.0, and 0.16 ± 0.02) and the D + L group (0.82 ± 0.05, 0.58 ± 0.09, and 0.15 ± 0.02) were significantly different than the d-gal group (0.67 ± 0.03, 0.96 ± 0.040, and 0.29 ± 0.05).Lidocaine was shown to reduce cognitive impairment in rats with cognitive dysfunction through anti-inflammatory and antioxidative stress mechanisms in combination with CRMP2 antiphosphorylation.© 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.