OBJECTIVE: To compare the effects of different chest compression rates (60-140 times/min) on hemodynamic parameters, return of spontaneous circulation (ROSC), resuscitation success, and survival in a porcine model of cardiac arrest (CA) followed by cardiopulmonary resuscitation (CPR). METHODS: Forty healthy male domestic pigs were randomly divided into five groups based on chest compression rate: 60, 80, 100, 120, and 140 times/min (n = 8). All animals underwent standard anesthesia and tracheal intubation. A catheter was inserted via the left femoral artery into the thoracic aorta to monitor aortic pressure (AOP), and another via the right external jugular vein into the right atrium to monitor right atrial pressure (RAP). In each group, animals were implanted with a stimulating electrode via the right external jugular vein to the endocardium, and ventricular fibrillation (VF) was induced by delivering alternating current stimulation, resulting in CA. After a 1-minute, manual chest compressions were performed at the assigned rate with a compression depth of 5 cm. The first defibrillation was delivered after 2 minutes of CPR. No epinephrine or other pharmacologic agents were administered during the entire resuscitation process. From 1 minute before VF induction to 10 minutes after ROSC, dynamic monitoring of AOP, coronary perfusion pressure (CPP), and partial pressure of end-tidal carbon dioxide (P_ETCO₂). Cortical ultrastructure was examined 24 hours post-ROSC using transmission electron microscopy. RESULTS: With increasing compression rates, both the total number of defibrillations and cumulative defibrillation energy significantly decreased, reaching their lowest levels in the 120 times/min group. The number of defibrillations decreased from (4.88±0.83) times in the 60 times/min group to (2.25±0.71) times in the 120 compressions/min group, and energy from (975.00±166.90)J to (450.00±141.42)J. However, both parameters increased again in the 140 times/min group [(4.75±1.04)times, (950.00±207.02)J], the differences among the groups were statistically significant (both P < 0.01). As compression frequency increased, P_ETCO₂, pre-defibrillation AOP and CPP significantly improved, peaking in the 120 times/min group [compared with the 60 times/min group, P_ETCO₂ (mmHg, 1 mmHg≈0.133 kPa): 18.69±1.98 vs. 8.67±1.30, AOP (mmHg): 95.13±7.06 vs. 71.00±6.41, CPP (mmHg): 14.88±6.92 vs. 8.57±3.42]. However, in the 140 times/min group, these values declined significantly again [P_ETCO₂, AOP, and CPP were (10.59±1.40), (72.38±11.49), and (10.36±4.57) mmHg, respectively], the differences among the groups were statistically significant (all P < 0.01). The number of animals achieving ROSC, successful resuscitation, and 24-hour survival increased with higher compression rates, reaching a peak in the 120 times/min group (compared with the 60 times/min group, ROSC: 7 vs. 2, successful resuscitation: 7 vs. 2, 24-hour survival: 7 vs.1), then decreased again in the 140 times/min group (the animals that ROSC, successfully recovered and survived for 24 hours were 3, 3, and 2, respectively). Transmission electron microscopy revealed that in the 60, 80, and 140 times/min groups, nuclear membranes in cerebral tissue were irregular and incomplete, nucleoli were indistinct, and mitochondria were swollen with reduced cristae and abnormal morphology. In contrast, the 100 times/min and 120 times/min groups exhibited significantly attenuated ultrastructural damage. CONCLUSIONS Among the tested chest compression rates of 60-140 times/min, a chest compressions frequency of 120 times/min is the most favorable hemodynamic profile and outcomes during CPR in a porcine CA model. However, due to the wide spacing between groups, further investigation is needed to determine the optimal compression rate range more precisely.
Animals ; Cardiopulmonary Resuscitation/methods* ; Swine ; Male ; Heart Arrest/therapy* ; Heart Massage/methods* ; Hemodynamics

OBJECTIVE: To investigate whether auraptene (AUR) exerts a protective effect on acute diquat (DQ)-induced liver injury in mice and explore its underlying mechanisms. METHODS: Forty SPF-grade healthy male C57BL/6 mice were randomly divided into normal control group (Control group), DQ poisoning model group (DQ group), AUR treatment group (DQ+AUR group), and AUR control group (AUR group), with 10 mice in each group. The DQ poisoning model was established via a single intraperitoneal injection of 40 mg/kg DQ aqueous solution (0.5 mL); Control group and AUR group received an equal volume of pure water intraperitoneally. Four hours post-modeling, DQ+AUR group and AUR group were administered 0.5 mg/kg AUR aqueous solution (0.2 mL) by gavage once daily for 7 consecutive days, while Control group and DQ group received pure water. Blood and liver tissues were collected after anesthesia on day 7. Liver ultrastructure was observed by transmission electron microscopy. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured via enzyme-linked immunosorbent assay (ELISA). Hepatic glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were detected using WST-1, thiobarbituric acid (TBA), and enzymatic reaction methods, respectively. Protein expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Kelch-like ECH-associated protein 1 (Keap1), and activated caspase-9 in liver tissues was analyzed by Western blotting. RESULTS: Transmission electron microscopy revealed that mitochondria in the Control group exhibited mild swelling, uneven distribution of matrix, and a small number of cristae fractures. In the AUR group, mitochondria showed mild swelling, with no obvious disruption of cristae structure. In the DQ group, mitochondria demonstrated marked swelling and increased volume, matrix dissolution, loss and fragmentation of cristae, and extensive vacuolization. In contrast, the DQ+AUR group showed significantly reduced mitochondrial swelling, volume increase, matrix dissolution, cristae loss and fragmentation, and vacuolization compared to the DQ group. Compared with the DQ group, the DQ+AUR group exhibited significantly lower serum AST levels (U/L: 173.45±23.60 vs. 255.33±41.51), ALT levels (U/L: 51.77±21.63 vs. 100.70±32.35), and hepatic MDA levels (μmol/g: 12.40±2.76 vs. 19.74±4.10), along with higher hepatic GSH levels (mmol/g: 37.65±14.95 vs. 20.58±8.52) and SOD levels (kU/g: 124.10±33.77 vs. 82.81±22.00), the differences were statistically significant (all P < 0.05). Western blotting showed upregulated Nrf2 expression (Nrf2/β-actin: 0.87±0.37 vs. 0.53±0.22) and HO-1 expression (HO-1/β-actin: 1.06±0.22 vs. 0.49±0.08), and downregulated Keap1 expression (Keap1/β-actin: 0.82±0.12 vs. 1.52±0.76) and activated caspase-9 expression (activated caspase-9/β-actin: 1.16±0.28 vs. 1.71±0.30) in the DQ+AUR group compared to the DQ group (all P < 0.05). CONCLUSION AUR attenuates DQ-induced acute liver injury in mice by activating the Keap1/Nrf2 signaling pathway.
Animals ; Male ; Mice ; Mice, Inbred C57BL ; Liver/pathology* ; Chemical and Drug Induced Liver Injury/drug therapy* ; Diquat/poisoning* ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; Apoptosis ; Coumarins

Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes, which seriously threatens the vision of patients. The pathogenesis of DR Is complex and involves many pathophysiological processes. At present, the treatment methods for DR Mainly include panretinal laser photocoagulation, vitrectomy and vitreous cavity injection, etc. However, each treatment method has certain limitations. In recent years, remarkable progress has been made in the field of drug treatment of DR, especially in anti-vascular endothelial growth factor drugs, anti-inflammatory drugs, anti-oxidative stress damage drugs, neuroprotective agents, gene therapy and stem cell therapy. These drugs not only improve the effectiveness of treatment, but also expand the range of treatment options. In addition, by carrying DR Treatment drugs on carriers such as nanoparticles, hydrogels and photosensitive materials, continuous and efficient release of drugs in the eye is achieved, thereby extending the time interval of administration and reducing the need for frequent treatment of patients. In the future, based on biomarker detection technology, it is expected to promote the development of personalized and precise treatment, which can develop more accurate treatment plans for patients and improve the efficacy.

Single-cell RNA sequencing (scRNA-seq) is an unbiased, high-throughput, and high-resolution transcriptome analysis method at the single-cell level.Unlike ordinary transcriptome sequencing, which study the average gene expression of all cells in tissues, scRNA-seq maps RNA to individual cells, which can be used to discover new cell types, reveal cell heterogeneity, and identify rare cells.Recently, more and more researches on scRNA-seq have focused on ophthalmology.This technology is expected to reveal the complex developmental biological processes of the retina and the pathogenesis of diseases, providing guidance for the clinical treatment of ophthalmology.This article briefly introduces the development and technical process of scRNA-seq, describes the identification of various retinal cell subtypes, the retinal cell development, and the application of retinal organoids in detail.This article systematically summarizes the latest research progress on scRNA-seq in the pathogenesis, diagnosis and treatment of retinal diseases, such as diabetic retinopathy and age-related macular degeneration, which mainly focuses on changes in cell-specific molecules and regulatory pathways in the occurrence and development of diseases, which will be helpful to search for potential new treatment targets for retinal diseases.

Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes, which seriously threatens the vision of patients. The pathogenesis of DR Is complex and involves many pathophysiological processes. At present, the treatment methods for DR Mainly include panretinal laser photocoagulation, vitrectomy and vitreous cavity injection, etc. However, each treatment method has certain limitations. In recent years, remarkable progress has been made in the field of drug treatment of DR, especially in anti-vascular endothelial growth factor drugs, anti-inflammatory drugs, anti-oxidative stress damage drugs, neuroprotective agents, gene therapy and stem cell therapy. These drugs not only improve the effectiveness of treatment, but also expand the range of treatment options. In addition, by carrying DR Treatment drugs on carriers such as nanoparticles, hydrogels and photosensitive materials, continuous and efficient release of drugs in the eye is achieved, thereby extending the time interval of administration and reducing the need for frequent treatment of patients. In the future, based on biomarker detection technology, it is expected to promote the development of personalized and precise treatment, which can develop more accurate treatment plans for patients and improve the efficacy.

Single-cell RNA sequencing (scRNA-seq) is an unbiased, high-throughput, and high-resolution transcriptome analysis method at the single-cell level.Unlike ordinary transcriptome sequencing, which study the average gene expression of all cells in tissues, scRNA-seq maps RNA to individual cells, which can be used to discover new cell types, reveal cell heterogeneity, and identify rare cells.Recently, more and more researches on scRNA-seq have focused on ophthalmology.This technology is expected to reveal the complex developmental biological processes of the retina and the pathogenesis of diseases, providing guidance for the clinical treatment of ophthalmology.This article briefly introduces the development and technical process of scRNA-seq, describes the identification of various retinal cell subtypes, the retinal cell development, and the application of retinal organoids in detail.This article systematically summarizes the latest research progress on scRNA-seq in the pathogenesis, diagnosis and treatment of retinal diseases, such as diabetic retinopathy and age-related macular degeneration, which mainly focuses on changes in cell-specific molecules and regulatory pathways in the occurrence and development of diseases, which will be helpful to search for potential new treatment targets for retinal diseases.

Objective:To investigate the regulatory effect of transient receptor potential cation channel subfamily C member 3 (TRPC3) on the retina in oxygen-induced retinopathy (OIR) mice and biological behavior of human retinal vascular endothelial cells (HREC).Methods:A total of 32 healthy SPF grade 7-day-old C57BL/6 mice were selected and randomly divided into a control group and an OIR group by the random number table method, with 16 mice in each group.The control group received no special treatment, and the OIR model was established in the OIR group.On postnatal day 17 (PN17), the success of the model establishment was verified by immunofluorescence staining of the retinal patch.The in vitro cultured HREC were divided into a normal control group, a transfection reagent group, and a si-TRPC3 group.The normal control group received no special treatment, while the transfection reagent group and the si-TRPC3 group were transfected with transfection reagent or transfection reagent + si-TRPC3.The relative expression of TRPC3 mRNA was detected by real-time quantitative fluorescence PCR.The relative expressions of TRPC3, transcription factor NF-E2 related factor (Nrf2), and superoxide dismutase (SOD) proteins were determined by Western blot.HREC were further divided into a normal control group, a vascular endothelial growth factor (VEGF) group, a si-TRPC3 group, and a Pyr3 (TRPC3 channel inhibitor) group, which were cultured in complete medium, medium containing 20 ng/ml VEGF recombinant protein, medium containing 20 ng/ml VEGF recombinant protein (si-TRPC3 transfection for 72 hours), and medium containing 20 ng/ml VEGF recombinant protein+ 1 μmol/L Pyr3 for 48 hours, respectively.The proliferation ability of HREC was detected using cell counting kit 8 (CCK-8). The horizontal and vertical migration ability of cells were detected by cell scratch assay and transwell assay, respectively.This study followed the 3R principles of animal welfare and was approved by the Ethics Committee of Hebei Eye Hospital (No.2023LW04). Results:Pathological neovascular clusters with strong fluorescent staining appeared in the retina of OIR mice on PN17.The relative expressions of TRPC3 mRNA and protein in the retina of OIR mice were 2.057±0.244 and 1.517±0.290, respectively, significantly higher than 0.983±0.033 and 0.874±0.052 of control group ( t=6.165, 3.094; both at P<0.05). The relative expression levels of TRPC3 mRNA and protein were significantly lower, and the relative expression levels of Nrf2 and SOD proteins were higher in the si-TRPC3 group than in the normal control and transfection reagent groups, and the differences were statistically significant (all at P<0.05). The CCK-8 experiment results showed that the cell absorbance value was higher in the VEGF group than in the normal control group, and lower in the si-TRPC3 and Pyr3 groups than in the VEGF group, with statistically significant differences (all at P<0.05). The results of the cell scratch experiment showed that the lateral migration rate of VEGF group cells was higher than that of normal control group, while the lateral migration rate of si-TRPC3 group and Pyr3 group cells was lower than that of VEGF group, and the differences were statistically significant (all at P<0.05). The transwell experiment results showed that the number of stained cells in the VEGF group was higher than that in the normal control group, and the number of stained cells in the si-TRPC3 group and Pyr3 group was lower than that in the VEGF group, with statistically significant differences (all at P<0.05). Conclusions:Hypoxia induces increased TRPC3 expression in OIR mouse retina, and downregulation of TRPC3 inhibits HREC proliferation and migration.The mechanism is related to the activation of the Nrf2-related oxidative stress pathway.

OBJECTIVE: To investigate the protective effect and mechanism of tumor necrosis factor receptor-associated factor 6 (TRAF6) inhibitor C25-140 on acute kidney injury (AKI) induced by acute diquat (DQ) poisoning in mice. METHODS: A total of 80 SPF grade healthy male C57BL/6 mice were randomly divided into the normal control group, DQ model group, C25-140 intervention group, and C25-140 control group, with 20 mice in each group. The DQ poisoning mouse model was established by using one-time intraperitoneal injection of 1 mL of 40 mg/kg DQ solution. The normal control group and C25-140 control group were injected with an equal amount of pure water into the peritoneal cavity. After 4 hours of model establishment, the C25-140 intervention group and C25-140 control group were given intraperitoneal injection of C25-140 5 mg/kg. The normal control group and DQ model group were given equal amounts of pure water, once a day for 7 consecutive days. After 7 days, the mice were anesthetized, eye blood was collected, and renal tissue was collected after sacrifice. The pathological changes of renal tissue were observed under a light microscope and renal tissue structure and mitochondrial changes were observed under transmission electron microscopy. The levels of serum creatinine (SCr) and blood urea nitrogen (BUN) were measured. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of serum interleukins (IL-6, IL-1β) and tumor necrosis factor-α (TNF-α). Western blotting was used to detect the protein expression levels of TRAF6, myeloid differentiation factor 88 (MyD88), and nuclear factor-κB (NF-κB) in renal tissue. Chemical method was used to determine the content of serum malondialdehyde (MDA) and superoxide dismutase (SOD). RESULTS: During the observation period, there were no abnormal behaviors in the normal control group mice. The DQ model group mice gradually showed symptoms such as mental fatigue, fluffy fur, reduced activity, and low food intake after being exposed to the toxin, and severe cases resulted in death. The above symptoms were alleviated in the C25-140 intervention group compared to the DQ model group. Under light microscopy, HE staining showed infiltration of inflammatory cells, glomerulosclerosis, proximal tubular dilation, and vacuolization in the DQ model group, while the inflammatory response was reduced in the C25-140 intervention group compared to the DQ model group. Under transmission electron microscopy, the DQ model group showed relatively high levels of mitochondrial damage, severe swelling, increased volume, matrix dissolution, ridge fracture and loss. The degree of mitochondrial damage in the C25-140 intervention group was reduced compared to the DQ model group. Compared with the normal control group, the levels of serum SCr, BUN, IL-6, IL-1β, TNF-α, and MDA in the DQ model group were significantly increased, while the serum SOD level was significantly decreased. Compared with the DQ model group, the levels of serum SCr, BUN, IL-6, IL-1β, TNF-α, and MDA in the C25-140 intervention group were significantly reduced [SCr (μmol/L): 59.07±13.11 vs. 83.61±20.13, BUN (mmol/L): 25.83±9.95 vs. 40.78±11.53, IL-6 (ng/L): 40.76±7.03 vs. 83.33±21.83, IL-1β (ng/L): 53.87±7.82 vs. 91.74±12.53, TNF-α (ng/L): 102.52±32.13 vs. 150.92±31.75, MDA (μmol/L): 3.57±1.06 vs. 5.75±1.83], and the serum SOD level was significantly increased (kU/g: 162.52±36.13 vs. 122.72±22.13), and the differences were statistically significant (all P < 0.01). Western blotting results showed that the protein expression levels of TRAF6, NF-κB, and MyD88 in the renal tissue of DQ model group mice were significantly higher than those in the normal control group. The expression levels of the above-mentioned proteins in the C25-140 intervention group of mice were significantly lower than those in the DQ model group (TRAF6/β-actin: 1.05±0.36 vs. 1.74±0.80, NF-κB/β-actin: 0.57±0.07 vs. 1.03±0.75, MyD88/β-actin: 0.58±0.07 vs. 1.03±0.33, all P < 0.05). CONCLUSIONS TRAF6 inhibitor C25-140 can alleviate AKI induced by DQ poisoning in mice by regulating the Toll-like receptor 4 (TLR4)/TRAF6/NF-κB signaling pathway and downregulating the levels of inflammatory cytokines IL-1β, IL-6, and TNF-α.
Animals ; Male ; Acute Kidney Injury/prevention & control* ; Mice ; Mice, Inbred C57BL ; Diquat ; TNF Receptor-Associated Factor 6/metabolism* ; Interleukin-6/blood* ; Kidney/pathology* ; NF-kappa B/metabolism* ; Peptide Fragments

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.

Objective:To investigate the protective effect of quercetin (QR) on acute liver injury induced by diquat (DQ) poisoning in mice and its mechanism.Methods:Eighty healthy male C57BL/6 mice with SPF grade were randomly divided into control group, DQ model group, QR treatment group, and QR control group, with 20 mice in each group. The DQ poisoning model was established by a one-time intraperitoneal injection of DQ solution (40 mg/kg); the control and QR control groups received equivalent amounts of distilled water through intraperitoneal injection. Four hours after modeling, the QR treatment group and the QR control group received 0.5 mL QR solution (50 mg/kg) through gavage. Meanwhile, an equivalent amount of distilled water was given orally to the control group and the DQ model group. The treatments above were administered once daily for seven consecutive days. Afterwards, the mice were anesthetized, blood and liver tissues were collected for following tests: changes in the structure of mice liver tissue were observed using transmission electron microscopy; the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected using enzyme linked immunosorbent assay (ELISA); the levels of glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) in liver tissues were measured using the water-soluble tetrazolium-1 (WST-1) method, the thiobarbituric acid (TBA) method, and enzymatic methods, respectively; the protein expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Kelch-like ECH-associated protein 1 (Keap1), and activated caspase-9 in liver tissues were detected using Western blotting.Results:Severe mitochondrial damage was observed in the liver tissues of mice in the DQ model group using transmission electron microscopy, yet mitochondrial damage in the QR treatment group showed significant alleviation. Compared to the control group, the DQ model group had significantly increased levels of MDA in liver tissue, serum AST, and ALT, yet had significantly decreased levels of GSH and SOD in liver tissue. In comparison to the DQ model group, the QR treatment group exhibited significant reductions in serum levels of ALT and AST, as well as MDA levels in liver tissue [ALT (U/L): 52.60±6.44 vs. 95.70±8.00, AST (U/L): 170.45±19.33 vs. 251.10±13.09, MDA (nmol/mg): 12.63±3.41 vs. 18.04±3.72], and notable increases in GSH and SOD levels in liver tissue [GSH (μmol/mg): 39.49±6.33 vs. 20.26±3.96, SOD (U/mg): 121.40±11.75 vs. 81.67±10.01], all the differences were statistically significant (all P < 0.01). Western blotting results indicated that the protein expressions of Nrf2 and HO-1 in liver tissues of the DQ model group were significantly decreased compared to the control group. On the other hand, the protein expressions of Keap1 and activated caspase-9 were conspicuously higher when compared to the control group. In comparison to the DQ model group, the QR treatment group showed a significant increase in the protein expressions of Nrf2 and HO-1 in liver tissues (Nrf2/β-actin: 1.17±0.08 vs. 0.92±0.45, HO-1/β-actin: 1.53±0.17 vs. 0.84±0.09). By contrast, there was a notable decrease in the protein expressions of Keap1 and activated caspase-9 (Keap1/β-actin: 0.48±0.06 vs. 1.22±0.09, activated caspase-9/β-actin: 1.17±0.12 vs. 1.59±0.30), the differences were statistically significant (all P < 0.01). Conclusion:QR may reduce acute liver injury induced by DQ poisoning in mice via activating Keap1/Nrf2 signaling pathway.