The retina has a complex and delicate function and structure, containing a large number of neuronal cells with extremely limited regenerative capacity, which are susceptible to damage and apoptosis under pathological conditions such as ischemia and hypoxia, resulting in irreversible vision loss. Retinal diseases are very common, such as retinitis pigmentosa(RP), age-related macular degeneration(ARMD), diabetic retinopathy(DR), and glaucoma. Most of the diseases in this category are treated symptomatically, which is effective but has some limitations in neuroprotection. Vascular endothelial growth factor(VEGF)-B is functionally relatively inert in the VEGF family, and unlike pro-angiogenic VEGF-A, VEGF-B shows functional inertia in angiogenesis but exhibits significant neuroprotective effects. VEGF-B is a potent anti-apoptotic, antioxidant factor that can regulate the expression of apoptotic genes and enhance the expression of glutamic acid decarboxylase 1 by binding to VEGFR-1 to activate the ERK1/2 or Akt pathway, in addition to decreasing the expression of glutamate, resulting in retinal neuroprotective effects. In this article, the protective effects of VEGF-B on retinal neuronal cells were reviewed to provide new ideas for the treatment of retina-associated diseases.

Background Environmental noise pollution is serious, and there are few studies on the effects of long-term noise exposure during sleep on cognitive function and possible biological clock mechanism. Objective To explore the cognitive impairment induced by noise exposure during sleep in mice and possible biological clock mechanism, and to provide a theoretical basis for the protection against noise exposure. Methods Twenty male C57BL/6J mice were randomly divided into a control group and a noise-exposed group, 10 mice in each group. The noise-exposed group was exposed to sleep-period noise using a noise generator for 12 h (08:00–20:00) per day for a total of 30 d. The calibrated noise intensity was set at 90 dB. No intervention was imposed on the control group. At the end of the noise exposure, cognitive function of mice was examined using the new object recognition experiment and the open field test, and the hippocampal tissue damage of mice were evaluated by Nissl staining, ionized calcium binding adaptor molecule 1 (Iba1) immunofluorescence staining, and real-time fluorescence quantitative PCR for inflammatory factors and biological clock genes. Oxidative stress indicators in the hippocampus of mice were also detected by assay kit. Results After noise exposure during sleep period, the results of new object recognition experiment showed that the discrimination index of mice in the noise-exposed group was 0.06±0.04, which was significantly lower than that of the control group (0.65±0.13) (P<0.05). The results of open field test showed that the central activity distance of the noise-exposed group was (242.20±176.10) mm, which was significantly lower than that of the control group, (1548.00±790.30) mm (P < 0.05), and the central activity time of the noise-exposed group was (0.87±0.64) s, which was significantly lower than that of the control group, (6.00±2.86) s (P < 0.05). The Nissl staining results showed that compared with the control group, neurons in the hippocampus of the noise-exposed mice were shrunken, deeply stained, disorganized, and loosely connected. The immunofluorescence results showed that microglia in the hippocampus of the noise-exposed mice were activated and the expression of Iba1 was significantly increased compared with those of the control group (P<0.05). The real-time PCR results of showed that the mRNA levels of the biological clock genes Clock, Per2, and Rev-erbα were significantly increased compared with those of the control group (P<0.05), and the mRNA level of Per1 was significantly decreased compared with that of the control group (P<0.05); and the mRNA levels of IL-18, IL-6, iNOS, and NLRP3 in the hippocampal tissues of mice were significantly increased compared with those of the control group (P<0.05). The results of oxidative stress evaluation showed that compared with the control group, reduced glutathione content was significantly reduced in the noise-exposed group (P<0.001). Conclusion Noise exposure during sleep period can lead to the destabilization of biological clock genes in hippocampal tissues and trigger hippocampal neuroinflammation, which can lead to the activation of microglia and cause cognitive impairment in mice.

Objective To investigate the peripheral retinal defocus and its influencing factors in children and adoles-cents with low to moderate myopia.Methods Totally 281 children and adolescents aged 6-15 years were included in the study,and only the right eye was selected.After cycloplegic refraction as well as axial length(AL)and average corneal curvature(AveK)measurements,the patients were divided into low myopia(LM)group(-3.00 D≤SE≤-0.50 D)and moderate myopia(MM)group(-6.00 D≤SE＜-3.00D)according to spherical equivalent(SE),and stratified compari-sons were made according to AL[AL1 group(23.00 mm≤AL≤24.00 mm),AL2 group(24.00 mm＜AL≤25.00 mm),and AL3 group(25.00 mm＜AL≤26.00 mm)]and AveK[AveK1 group(40.00 D≤ Ave K≤43.00 D)and AveK2 group(43.00 D＜AveK≤46.00 D)].Multispectral refraction tomography was used to measure the refraction difference value(RDV),in-cluding TRDV(0° to 53°),RDV-15(0° to 15°),RDV-30(0° to 30°),RDV-45(0° to 45°),RDV-15-30(15° to 30°),RDV-30-45(30° to 45°),RDV-45-53(45° to 53°),RDV-S(superior),RDV-I(inferior),RDV-T(temporal)and RDV-N(na-sal).The RDV was compared in the groups divided according to SE,AL and AveK individually,and the correlation be-tween RDV and age,SE,AL and AveK was analyzed.Moreover,the factors affecting RDV in all ranges were analyzed by multiple linear regression.Results Compared with the LM group,the MM group had significant increases in TRDV,RDV-30,RDV-45,RDV-15-30,RDV-30-45,RDV-45-53,RDV-S,RDV-I and RDV-N(all P＜0.05)and no significant differ-ence in RDV-15 and RDV-T(both P＞0.05).According to the comparisons of AL groups and AveK groups,the TRDV,RDV-30,RDV-45,RDV-15-30,RDV-30-45,RDV-45-53,RDV-S,RDV-I and RDV-N in the AL2 group were significantly higher than those in the AL1 group(all P＜0.05);the TRDV,RDV-30,RDV-45,RDV-15-30,RDV-30-45,RDV-45-53,RDV-S and RDV-N in the AL3 group were significantly higher than those in AL2 and AL1 groups,and RDV-I and RDV-T in the AL3 group were significantly higher than those in the AL1 group(both P＜0.05);the TRDV,RDV-30,RDV-45,RDV-15-30,RDV-30-45,RDV-45-53,RDV-S,and RDV-I in the Ave K1 group were significantly higher than those in the AveK2 group(all P＜0.05).The correlation analysis showed that TRDV,RDV-45,RDV-30-45,RDV-45-53,RDV-S and RDV-N were positively correlated with age and AL and negatively correlated with SE and Ave K;RDV-30,RDV-15-30 and RDV-I were positively cor-related with AL and negatively correlated with SE and AveK;RDV-T was positively correlated only with AL;RDV-15 was not correlated with age,SE,AL and AveK.Multiple linear regression analysis showed that age was the influencing factor of RDV-45-53 and RDV-S;AL was the influencing factor of TRDV,RDV-30,RDV-45,RDV-15-30,RDV-30-45,RDV-45-53,RDV-S and RDV-T;AveK was the influential factor of RDV-I;SE had no significant effect on RDV in all ranges.Conclu-sion Peripheral retinal defocus in children and adolescents with low to moderate myopia has reached hyperopic defocus,and hyperopic defocus is the least in patients with relatively short AL.Age,AL and AveK can affect peripheral retinal defo-cus in children and adolescents with low to moderate myopia,among which AL is the most important influencing factor.

Objective:To identify the key genes in the process inhibiting inflammation by overexpression adenovirus-mediated pigment epithelium-derived factor ( PEDF) gene in human monocytic leukemia cells THP1. Methods:Proteomic analysis of THP1 overexpressing adenovirus-mediated PEDF gene was performed.The THP1 cells were divided into GFP and PEDF groups, transfected with GFP and PEDF adenovirus, respectively.The THP1 cells were divided into mannitol group, high glucose group, high glucose+ GFP group, and high glucose+ PEDF group, which were cultured with mannitol for 4 days, anhydrous glucose for 4 days, GFP adenovirus for 3 days, and PEDF adenovirus for 3 days, respectively.The Pedf-/- mice were divided into Pedf-/- group and Pedf-/- diabetes group according to the random table method, with 12 mice in each group.Another 10 C57BL/6 mice were taken as the control group.Mouse retinas were collected for experiments.The mRNA expression levels of differentially expressed genes (DEGs) in retina and THP1 cells were verified by real-time fluorescence quantitative PCR.The DEGs were intersected with the GSE5504 dataset, and the protein-protein interaction (PPI) network was built using the String database.Modules of the PPI were extracted using the Cytoscape software and the MCODE application.Intersections were taken with the Set1 dataset and key genes were found.The expression levels of key genes in THP1 cells and Pedf-/- mice were verified by Western blot.The feeding and operation of experimental animals were in accordance with the regulations of the State Science and Technology Commission on the management of experimental animals and approved by the Animal Management and Use Committee of Tianjin Medical University (No.TTYY2023120217). Results:Through proteomics and bioinformatics analysis, 105 DEGs in the Set1 dataset were screened.The results of real-time PCR showed that the relative expression levels of ARF5, TCF25 and KCTD9 mRNA were significantly higher and the relative expression levels of RNPS1, CSF1R, OGA, IBA57 and MGST2 mRNA were significantly lower in PEDF group than in GFP group, showing statistically significant differences (all at P<0.001).There were significant overall differences in the relative expression levels of down-regulated TCF25, KCTD9 and ARF5 mRNA and up-regulated CSF1R, RNPS1 and IBA57 mRNA among control group, Pedf-/- group and Pedf-/- diabetes group ( F=64.057, 27.561, 37.179, 65.757, 44.024, 34.248; all at P<0.001).Compared with control group, the relative expression levels of TCF25, KCTD9 and ARF5 mRNA were decreased and the relative expression levels of CSF1R and RNPS1 mRNA were increased in Pedf-/- group, showing statistically significant differences (all at P<0.05).Compared with control group, the relative expression levels of TCF25, KCTD9 and ARF5 mRNA were decreased and the relative expression levels of CSF1R, RNPS1 and IBA57 mRNA were increased in Pedf-/- diabetes group, showing statistically significant differences (all at P<0.05).Compared with Pedf-/- group, the relative expression level of TCF25 mRNA was decreased and the relative expression levels of CSF1R, RNPS1 and IBA57 mRNA were increased in Pedf-/- diabetes group, showing statistically significant differences (all at P<0.05).After intersection with the GSE5504 dataset, 20 differential proteins were obtained, which were mainly enriched in positive regulation of gene expression, positive regulation of ERK1 and ERK2 cascade, positive regulation of insulin secretion involved in cell response to glucose stimulation and antigen processing and presentation pathways.The key gene CSF1R was screened by constructing PPI network and MCODE plugin in Cytoscape software.Western blot results showed that the expression levels of CSF1R in high glucose group and high glucose+ GFP group were 1.961±0.085 and 1.000±0.069, which were higher than 1.000±0.072 in mannitol group and 0.469±0.079 in high glucose+ PEDF group, respectively, and the differences were statistically significant ( t=14.940, 8.765; both at P < 0.01).The expression of CSF1R in the retina of Pedf-/- diabetes group was 1.633±0.192, which was higher than 1.000±0.050 in Pedf-/- group, and the difference was statistically significant ( t=5.537, P<0.01). Conclusions:CSF1R may be a key gene and therapeutic target for the inhibition of inflammation by overexpression of adenovirus-mediated PEDF gene in THP1 cell.

Background Previous research indicated that isomers and alternatives of per- and polyfluoroalkyl substances (PFAS) probably disturb glucose metabolism; however, current epidemiological evidence on the associations of PFAS with fasting blood glucose is inconsistent. Besides, studies on the joint association of multiple components of PFAS and fasting blood glucose as well as the key component are scarce. Objective To evaluate the associations of PFAS isomers and alternatives with fasting blood glucose and their joint effects, as well as identify the key component among population without glucose metabolism problems. Methods We selected 923 adults without glucose metabolism problems or missing data from the Isomers of C8 Health Project in China (2015—2016). Serum PFAS isomers and alternatives and fasting blood glucose were measured using ultra-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) and automatic biochemical analyzer. We applied multiple linear regression to explore the associations of 16 pollutants which were detected among over 80% participants with fasting blood glucose. Meanwhile, we utilized qgcomp and Bayesian kernel machine regression (BKMR) models to explore the joint effects of PFAS isomers and alternatives mixture on target outcome indicators and identify the key component. Results The average age among the 923 participants in this study was (62.4±13.8) years old, including 472 men (51.1%) and 451 women (48.9%). Among selected PFAS isomers and alternatives, the highest serum concentration was ∑3+4+5m-PFOS (perfluoro-3/4/5-methylheptanesulfonate) with a median concentration of 10.20 ng·mL⁻¹. The concentrations of linear perfluorooctane sulfonate (n-PFOS, 9.61 ng·mL⁻¹), perfluorooctanoic acid (PFOA, 4.55 ng·mL⁻¹), linear perfluorohexane sulfonic acid (n-PFHxS, 2.48 ng·mL⁻¹), 6:2 chlorinated polyfluorinated ethersulfonic acid (6:2 Cl-PFESA, 1.90 ng·mL⁻¹), perfluoro-6-methylheptanesulfonate (iso-PFOS, 1.85 ng·mL⁻¹), perfluorobutanoic acid (PFBA, 1.81 ng·mL⁻¹), perfluorinated n-nonanoic acid (PFNA, 1.39 ng·mL⁻¹), and perfluoro-1-methylheptanesulfonate (1m-PFOS, 1.27 ng·mL⁻¹) were higher than 1.00 ng·mL⁻¹. After being adjusted for selected confounders, PFAS isomers and alternatives were positively associated with fasting blood glucose. With 1 ln unit concentration increment of 6:2 Cl-PFESA and PFNA, the estimated changes of fasting blood glucose were 0.18 (95%CI: 0.13, 0.23) mmol·L⁻¹ and 0.24 (95%CI: 0.18, 0.30) mmol·L⁻¹, respectively. The multi-pollutant models indicated a joint association of PFAS isomers and alternatives mixture with fasting blood glucose. The BKMR models reveals that as the quantiles of mixture elevated from the 50^th to the 75^th percentile, the values of fasting blood glucose increased 0.25 (95%CI: 0.21, 0.30) mmol·L⁻¹, and the posterior inclusion probability of PFNA was 0.92, implying that PFNA was the key component. Conclusion PFAS isomers and alternatives are positively associated with fasting blood glucose. PFNA is the key component of the joint association.

OBJECTIVE：To study the effects of virus in activation treatment of plasma specimen on plasma concentration determination of voriconzole ，linezolid，vancomycin and teicoplanin. METHODS ：The remaining plasma of 36 inpatients in our hospital after routine blood concentration examination of voriconazole ，linezolid，vancomycin and teicoplanin were collected as specimen（9 drug-contained plasma specimens for each drug ），and merged into three different concentration levels （low，medium， high）of mixed samples according the results of routine blood test. Then the mixed samples with different concentration levels were divided into inactivated group and non-inactivated group ，with 3 samples in each group. The inactivated plasma samples were heated at 56 ℃ for 30 min in metal bath with constant temperature. Non-inactivated group were not treated. After pretreating plasma sample of 2 groups，2-dimensional liquid chromatography was used to detect plasma concentration of the four drugs ；the difference of detection result between inactivated group and non-inactivated group were analyzed. RESULTS ：Plasma samples containing voriconazole，linezolid，vancomycin and teicoplanin were still stable after heating at 56 ℃ for 30 min in metal bath with constant temperature. Compared with non-inactivated group ，relative error of plasma concentration detection result of above 4 drugs were all lower than 15％ in low ，medium，high concentration mixed samples of inactivated group. CONCLUSIONS ：Plasma samples can be inactivated by heating at 56 ℃ for 30 min in metal bath with constant temperature ，when the plasma concentration of voriconazole，linezolid，vancomycin and teicoplanin are determined by 2-dimensional liquid chromatography.

Objective:To compare the difference of low-level assisted ventilation and T-piece method on respiratory mechanics of patients with invasive mechanical ventilation during spontaneous breathing trial (SBT) within 3 days before extubation.Methods:A retrospective observational study was conducted. Twenty-five patients with difficulty in weaning or delayed weaning from invasive mechanical ventilation who were admitted to department of critical care medicine of the First Affiliated Hospital of Guangzhou Medical University from December 2018 to June 2020, and were in stable condition and entered the weaning stage after more than 72 hours of invasive mechanical ventilation were studied. A total of 119 cases of respiratory mechanical indexes were collected, which were divided into the low-level assisted ventilation group and the T-piece group according to the ventilator method and parameters used during the data collection. The different ventilation modes related respiratory mechanics indexes such as the esophageal pressure (Pes), the gastric pressure (Pga), the transdiaphragmatic pressure (Pdi), the maximum Pdi (Pdimax), Pdi/Pdimax ratio, the esophageal pressure-time product (PTPes), the gastric pressure-time product (PTPga), the transdiaphragmatic pressure-time product (PTPdi), the diaphragmatic electromyography (EMGdi), the maximum diaphragmatic electromyography (EMGdimax), PTPdi/PTPes ratio, Pes/Pdi ratio, the inspiratory time (Ti), the expiratory time (Te) and the total time respiratory cycle (Ttot) at the end of monitoring were recorded and compared between the two groups.Results:Compared with the T-piece group, Pes, PTPes, PTPdi/PTPes ratio, Pes/Pdi ratio and Te were higher in low-level assisted ventilation group [Pes (cmH 2O, 1 cmH 2O = 0.098 kPa): 2.84 (-1.80, 5.83) vs. -0.94 (-8.50, 2.06), PTPes (cmH 2O·s·min -1): 1.87 (-2.50, 5.93) vs. -0.95 (-9.71, 2.56), PTPdi/PTPes ratio: 0.07 (-1.74, 1.65) vs. -1.82 (-4.15, -1.25), Pes/Pdi ratio: 0.17 (-0.43, 0.64) vs. -0.47 (-0.65, -0.11), Te (s): 1.65 (1.36, 2.18) vs. 1.33 (1.05, 1.75), all P < 0.05], there were no significant differences in Pga, Pdi, Pdimax, Pdi/Pdimax ratio, PTPga, PTPdi, EMGdi, EMGdimax, Ti and Ttot between the T-piece group and the low-level assisted pressure ventilation group [Pga (cmH 2O): 6.96 (3.54,7.60) vs. 7.74 (4.37, 11.30), Pdi (cmH 2O): 9.24 (4.58, 17.31) vs. 6.18 (2.98, 11.96), Pdimax (cmH 2O): 47.20 (20.60, 52.30) vs. 29.95 (21.50, 47.20), Pdi/Pdimax ratio: 0.25 (0.01, 0.34) vs. 0.25 (0.12, 0.41), PTPga (cmH 2O·s·min -1): 7.20 (2.54, 9.97) vs. 7.97 (5.74, 13.07), PTPdi (cmH 2O·s·min -1): 12.15 (2.95, 19.86) vs. 6.87 (2.50, 12.63), EMGdi (μV): 0.05 (0.03, 0.07) vs. 0.04 (0.02, 0.06), EMGdimax (μV): 0.07 (0.05, 0.09) vs. 0.07 (0.04, 0.09), Ti (s): 1.20 (0.95, 1.33) vs. 1.07 (0.95, 1.33), Ttot (s): 2.59 (2.22, 3.09) vs. 2.77 (2.35, 3.24), all P > 0.05]. Conclusions:When mechanically ventilated patients undergo SBT, the use of T-piece method increases the work of breathing compared with low-level assisted ventilation method. Therefore, long-term use of T-piece should be avoided during SBT.

BACKGROUND: Chronic noise exposure is one environmental hazard that is associated with genetic susceptibility factors that increase Alzheimer's disease (AD) pathogenesis. However, the comprehensive understanding of the link between chronic noise stress and AD is limited. Herein, we investigated the effects of chronic noise exposure on AD-like changes in senescence-accelerated mouse prone 8 (SAMP8). METHODS: A total of 30 male SAMP8 mice were randomly divided into the noise-exposed group, the control group, and aging group (positive controls), and mice in the exposure group were exposed to 98 dB SPL white noise for 30 consecutive days. Transcriptome analysis and AD-like neuropathology of hippocampus were examined by RNA sequencing and immunoblotting. Enzyme-linked immunosorbent assay and real-time PCR were used to further determine the differential gene expression and explore the underlying mechanisms of chronic noise exposure in relation to AD at the genome level. RESULTS: Chronic noise exposure led to amyloid beta accumulation and increased the hyperphosphorylation of tau at the Ser202 and Ser404 sites in young SAMP8 mice; similar observations were noted in aging SAMP8 mice. We identified 21 protein-coding transcripts that were differentially expressed: 6 were downregulated and 15 were upregulated after chronic noise exposure; 8 genes were related to AD. qPCR results indicated that the expression of Arc, Egr1, Egr2, Fos, Nauk1, and Per2 were significantly high in the noise exposure group. These outcomes mirrored the results of the RNA sequencing data. CONCLUSIONS These findings further revealed that chronic noise exposure exacerbated aging-like impairment in the hippocampus of the SAMP8 mice and that the protein-coding transcripts discovered in the study may be key candidate regulators involved in environment-gene interactions.

Objective:To investigate the effects of early applying of basic fibroblast growth factor (bFGF) on corneal haze formation after surface ablation surgery in rabbits.Methods:The right eyes of 60 healthy New Zealand white rabbits received photorefractive keratectomy (PRK) and were randomized into PRK+ normal saline group, PRK+ bFGF group and simple PRK group, with 20 rabbits in each group.Normal saline solution and bFGF were topically administered according to grouping, respectively, 3 times per day, 1 drop for each time until the sacrifice of the animals, and no drug was used in the PRK group.Another 8 normal rabbits were served as blank control group.The corneal healing response and haze formation were evaluated by anterior segment photography and anterior segment optical coherence tomography (AS-OCT) and graded based on Fantes criteria.Corneal histopathology was examined by hematoxylin-eosin staining.Immunohistochemistry was used to detect the expression of transforming growth factor-β 1(TGF-β 1), α-smooth muscle actin (α-SMA) and matrix metalloproteinase-2 (MMP-2) in cornea.This study protocol was approved by the Experimental Animal Ethic Committee of Affiliated Hospital of Binzhou Medical University (20180209-03). The use and care of the animals complied with the Statement of ARVO. Results:The corneal epithelium was completely healed in 3-4 days following surgery and there was not significantly different in healing time among the three groups.( F=0.57, P=0.57). The haze grading was significantly different among different groups at different time points ( Fgroup=41.736, P<0.01; Ftime=129.445, P<0.01) and showed the highest score in the PRK+ bFGF group on the 28th day after operation.On the 7th day after surgery, AS-OCT image showed that the surface reflection of corneal epithelium was continuous and smooth and corneal epithelium was not tightly attached to the superficial stromal layer; the reflection of the superficial stromal layer was enhanced in all the operation groups.The proliferation of corneal epithelial cells and superficial stromal layer in the operation area were seen under the optical microscope, and the arrangement of collagen fibers in the stromal layer was disordered with the most obvious changes in the PRK+ bFGF group in comparison with the PRK+ normal saline group and the simple PRK group, and these findings became worse on postoperative 28 days.The corneal epithelial surface reflection in the blank control group was continuous and smooth.Immunohistochemistry showed that a few MMP-2 positive cells were seen in the blank control group.TGF-β 1, α-SMA and MMP-2 proteins were positively expressed in the corneas 7 days after surgery in the three groups, and their expressions were the most obvious in the PRK+ bFGF in comparison with the PRK+ normal saline group and the PRK group and were enhanced 28 days after operation, showing statistically differences (all at P<0.05). Conclusions:Early application of bFGF following surface ablation surgery promotes the proliferation of corneal epithelial cells and irregular arrangement of collagen in the superficial stromal layer, which is associated with the expressions of haze-related factors TGF-β 1, α-SMA and MMP-2 in corneas.

AIM: To investigate the PI3K/AKT/GSK-3β signaling pathway involved in the protective effect and mechanism of propofol on the cerebral ischemia-reperfusion injury in rats. METHODS: There were 72 healthy male SD rats. All rats established a model of focal cerebral ischemia-reperfusion injury according to the Zea Longa method and were randomly divided into six groups (n=12), A-sham operation group, B-model group (MCAO), C-Propofol group, D-Propofol+adenosine A1R antagonist group (DPCPX), E-Propofol group+PI3K specific inhibitor (LY294002), F-Propofol+GSK3β inhibitor group (SB216763). The neurological scores of rats 24 h after operation, LDF monitors changes in cerebral blood flow before and after embolization were observed. The TTC staining method was used to detect the cerebral infarction volume of rats in each group; HE staining method was used to observe the morphological changes of the rat brain tissue; Immunohistochemical method was used to detect Bcl-2 positive cells expression; TUNEL was used to detect cerebral cortex ischemia in each group. The percentage of neuronal apoptotic cells. RESULTS: Compared with group A, the behaviors, cerebral infarction volume, apoptosis rate, and Bcl-2 protein expression of rats in groups B, C, D, E, and F all increased (P<0.05); compared with group C, the behavioral scores, cerebral infarction volume and apoptosis rate of rats in groups B, D and E all increased significantly, and the expression of Bcl-2 protein was decreased significantly (P<0.01), but the expression of Bcl-2 protein in group F was increased, cell apoptosis rate decreased (P<0.05), behavior score and infarcts decreased (P<0.05). CONCLUSION: The neuroprotective effect of propofol mediated by adenosine A1R on ischemia-reperfusion injury in rats may be related to the PI3K/AKT/GSK-3β signal transduction pathway.