Neuropathic pain(NP)is caused by leision or disease of the somatic sensory nervous system,and its pathological mechanism is complex,mainly related to abnormal neural structure and function.It is hard for existing treatment methods to obtain satisfactory results.With the deepening of the study of peroxisome proliferate activation receptor-γ(PPAR-γ),its role in neuroinflammation,oxidative stress,ion channels,mitochondrial function,neuroprotection and other aspects have been discovered succes-sively,PPAR-γ may be one new target for pain prevention and treatment.This paper reviews the role of PPAR-γ in NP and related mechanisms,in order to provide new thinking for the clinical treatment of NP.

AIM:To investigate the effects and possible mechanisms of liraglutide on postopera-tive cognitive function in aged mice.METHODS:C57BL/6J male-aged mice were randomly divided into 4 groups:control group(N group),liraglutide group(L group),model group(M group),and mod-el+liraglutide group(ML group).There were 12 mice in each group.The model was constructed by using sevoflurane anesthesia combined with dis-secting the abdominal cavity in M and ML groups.In L and M groups,liraglutide was injected into the peritoneal cavity at 300 μg/kg,once per day,for 14 days.Postoperatively,the cognitive function of mice was detected by using the open field test,the Y maze experiment,and the conditioned fear ex-periment.Western blotting and ELISA were used to detect the expression of hippocampal glucagon-like peptide-1 receptor(GLP1R),β-arrestin2(β-arres-tin2),stimulator of interferon genes(STING),TANK-binding kinase 1(TBK1),IL-1β,and IL-6;immunoflu-orescence was used to observe the Iba1-positive microglial cell quantity.RESULTS:Compared with N group,M group showed a decrease in the postop-erative spontaneous alternation rate,percentage of freezing time,and GLP1R expression in hippocam-pal tissue(P＜0.05)and an increase in the expres-sion of β-arrestin2,STING,P-TBK1,IL-6,IL-1β,and the number of Iba1-positive cells(P＜0.05).Com-pared with M group,postoperative spontaneous al-ternation rate,percentage of freezing time,and GLP1R expression were increased in ML group(P＜0.05),and the number of β-arrestin2,P-TBK1,IL-6,IL-1β,and Iba1-positive cells was significantly de-creased in ML group(P＜0.05).CONCLUSION:Lira-glutide may ameliorate postoperative cognitive im-pairment in aged mice by inhibiting the β-arrestin2/STING/TBK1 pathway.

AIM:To investigate the effects and possible mechanisms of liraglutide on postopera-tive cognitive function in aged mice.METHODS:C57BL/6J male-aged mice were randomly divided into 4 groups:control group(N group),liraglutide group(L group),model group(M group),and mod-el+liraglutide group(ML group).There were 12 mice in each group.The model was constructed by using sevoflurane anesthesia combined with dis-secting the abdominal cavity in M and ML groups.In L and M groups,liraglutide was injected into the peritoneal cavity at 300 μg/kg,once per day,for 14 days.Postoperatively,the cognitive function of mice was detected by using the open field test,the Y maze experiment,and the conditioned fear ex-periment.Western blotting and ELISA were used to detect the expression of hippocampal glucagon-like peptide-1 receptor(GLP1R),β-arrestin2(β-arres-tin2),stimulator of interferon genes(STING),TANK-binding kinase 1(TBK1),IL-1β,and IL-6;immunoflu-orescence was used to observe the Iba1-positive microglial cell quantity.RESULTS:Compared with N group,M group showed a decrease in the postop-erative spontaneous alternation rate,percentage of freezing time,and GLP1R expression in hippocam-pal tissue(P＜0.05)and an increase in the expres-sion of β-arrestin2,STING,P-TBK1,IL-6,IL-1β,and the number of Iba1-positive cells(P＜0.05).Com-pared with M group,postoperative spontaneous al-ternation rate,percentage of freezing time,and GLP1R expression were increased in ML group(P＜0.05),and the number of β-arrestin2,P-TBK1,IL-6,IL-1β,and Iba1-positive cells was significantly de-creased in ML group(P＜0.05).CONCLUSION:Lira-glutide may ameliorate postoperative cognitive im-pairment in aged mice by inhibiting the β-arrestin2/STING/TBK1 pathway.

AIM: To investigate the relationship between human cholesteryl ester transfer protein CETP gene polymorphism and postoperative neurocognitive disorders (PND). METHODS: A total of 124 elderly patients over 65 years of age who underwent elective non-cardiac surgery were enrolled in the study while 25 healthy volunteers matching age and sex were recruited as the control group. Neuropsychological tests were performed 1 day before surgery, 7 days, and 3 months after surgery. PND was determined using the Z value method. The venous blood sample of the surgical patient was taken before the operation, followed by direct gene sequencing. Statistical methods were used to calculate the correlation between CETP gene polymorphism (rs5882) and PND. RESULTS: The incidence of PND was 29.3% and 18.2% at 7 days and 3 months after operation respectively. The A allele frequency of PND patients was significantly higher than that of non-PND patients 7 days and 3 months after surgery (65.52% vs. 41.43%, 34.48% vs. 58.57%, P=0.001), while the G allele frequency in PND group lower than that of non-PND (58.33% vs. 37.86%, 41.67% vs. 62.14%, P=0.004).AA genotype in PND patients was 34.48%, 38.89% at 7 days and 3 months after surgery respectively, significantly higher than 14.29%, 16.05% of non-PND (P=0.023, P=0.029). CONCLUSION: CETP rs5882 polymorphism is associated with PND and AA genotype may be a predisposing factor for postoperative PND in Chinese Han elderly patient.