Adenosine receptor A1 enhanced mitochondrial biogenesis and exerted neuroprotection after cerebral ischemia through PGC-1α.

Ischemic stroke is a common cause of morbidity and mortality worldwide. The current treatment fails to achieve satisfactory results, because interventional therapy as first-line treatment management has a strict time window. In recent years, a large number of studies have confirmed that adenosine, as an inhibitory neurotransmitter, has a protective effect on cerebral ischemic injury. Nevertheless, direct administration of adenosine has many side effects. Previous studies showed that adenosine exerted neuroprotective effects mainly through adenosine receptor A1 (A1 receptor). Therefore, further study on the mechanism of A 1 receptor induced neuroprotection may find new targets for stroke treament. Mitochondrial biogenesis (MB) is a therapeutic target for ischemic stroke, and the nuclear-encoded peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) is a major regulator of MB. However, the influence of A1 receptor on MB and PGC-1α is unclear. In this study, using the middle cerebral artery occlusion (MCAO) model of mice, we evaluated the temporal and spatial effects of A1 receptor after ischemic stroke and verified the neuroprotection of A1 receptor. Neurological scores were used to assess functional changes in mice. At the same time, we observed the effect of activating A1 receptor on MB and PGC-1α, and the effect of knockdown PGC-1α on A1 receptor induced MB in vitro. WB and immunofluorescence were used to detect relevant indicators of MB. In addition, we downregulated PGC-1α in vivo to observe the effects on A1 receptor induced MB and neuroprotection. The findings indicated that A1 receptor was increased and mainly expressed on neurons in the penumbra, further activated A1 receptor after stroke had neuroprotection. In vitro, activation of A1 promotes MB and increases the expression level of PGC-1α, while downregulation of PGC-1α partially reverses the effect of A1 receptor after OGD/R. Down regulation of PGC-1α in the penumbra neurons can reverse the effects of activation of A1 receptor on MB and neuroprotection. Taken together, these findings indicated that A1receptor promotes MB and improves neurological function after ischemic stroke via PGC-1α.

Compound lidocaine/prilocaine cream combined with tetracaine prevents cough caused by extubation after general anaesthesia: a randomised controlled trial.

BACKGROUND: Coughing caused by tracheal extubation is common following general anaesthesia. Heavy aerosol production by coughing during recovery from general anaesthesia in patients with respiratory infections (especially COVID-19) may be one of the highest risk factors for infection in healthcare workers. The application of local anaesthetics to the endotracheal tube is an effective method to reduce coughing. The most commonly used anaesthetics are compound lidocaine/prilocaine cream and tetracaine spray. However, coughing still occurs when the two anaesthetics are used alone. We speculated that the application of compound lidocaine/prilocaine combined with tetracaine spray would better prevent coughing caused by tracheal extubation. METHODS: Patients scheduled for laparoscopic cholecystectomy or cholecystectomy combined with common bile duct exploration under general anaesthesia were randomly assigned to Group C (saline spray), Group L (2 g compound lidocaine/prilocaine cream contains 5 mg of lidocaine and 5 mg prilocaine)), Group T (tetracaine) and Group F (compound lidocaine/prilocaine cream combined with tetracaine). The incidence of coughing, the endotracheal tube tolerance assessment, the incidence of agitation, the active extubation rate, the incidence of postoperative pharyngeal pain and the incidence of postoperative cough were recorded and analysed. Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and the plasma concentrations of epinephrine and norepinephrine were measured immediately before extubation and 1 min after extubation. RESULTS: A total of 211 patients were randomly assigned to Group C (53 cases), Group L (52 cases), Group T (52 cases) and Group F (54 cases). The primary result is assessment of the incidence of cough. The patients emerged from general anaesthesia, 96% of Group C had cough, which was significantly reduced in Group L (61.5%, P < 0.001), Group T (75%, P < 0.05) and Group F (22.2%, P < 0.001). Group F had a significantly reduced incidence of cough compared to Group L and Group T (P < 0.05 or P < 0.01, respectively). The secondary results were assessed. The endotracheal tube tolerance score in Group C ((1, 3) 4, P < 0.001) was higher than Group L ((0, 1) 2), Group T ((0, 1.25) 3) and Group F ((0, 0) 1). Group F had a significantly lower score than Group L and Group T (P < 0.05, P < 0.01, respectively). The incidence of agitation and the active extubation rate were also higher in Group C (96.2% and 71.7%, respectively, P < 0.001) than Group L (48.1% and 15.4%, respectively), Group T (61.5% and 26.9%, respectively) and Group F (17.3% and 7.7%, respectively). Blood pressure, HR and plasma concentrations of epinephrine and norepinephrine were significantly higher in Group C than in all other groups at the time of extubation and 1 min after extubation (P < 0.001). Group F exhibited significantly reduced blood pressure, heart rate and plasma concentrations of epinephrine and norepinephrine compared to Group L and Group T (P < 0.05, P < 0.01 or P < 0.001, respectively). The incidence of postoperative pharyngeal pain and the incidence of postoperative cough were not significantly different among the groups. CONCLUSIONS: Compound lidocaine/prilocaine cream combined with tetracaine may be a more effective approach for preventing coughing and stabilising circulation during extubation following general anaesthesia. This may play an important role in preventing medical staff from contracting respiratory infectious diseases. TRIAL REGISTRATION: Chinese Clinical Trial Registry: ChiCTR2200058429 (registration date: 09-04-2022) "retrospectively registered".

Edaravone alleviates cell apoptosis and mitochondrial injury in ischemia-reperfusion-induced kidney injury via the JAK/STAT pathway.

BACKGROUND: Kidney ischemia-reperfusion injury is a common pathophysiological phenomenon in the clinic. A large number of studies have found that the tyrosine protein kinase/signal transducer and activator of transcription (JAK/STAT) pathway is involved in the development of a variety of kidney diseases and renal protection associated with multiple drugs. Edaravone (EDA) is an effective free radical scavenger that has been used clinically for the treatment of postischemic neuronal injury. This study aimed to identify whether EDA improved kidney function in rats with ischemia-reperfusion injury by regulating the JAK/STAT pathway and clarify the underlying mechanism. METHODS: Histomorphological analysis was used to assess pathological kidney injury, and mitochondrial damage was observed by transmission electron microscopy. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining was performed to detect tubular epithelial cell apoptosis. The expression of JAK2, P-JAK2, STAT3, P-STAT3, STAT1, P-STAT1, BAX and Bcl-2 was assessed by western blotting. Mitochondrial function in the kidney was assessed by mitochondrial membrane potential (ΔΨm) measurement. RESULTS: The results showed that EDA inhibited the expression of p-JAK2, p-STAT3 and p-STAT1, accompanied by downregulation of the expression of Bax and caspase-3, and significantly ameliorated kidney damage caused by ischemia-reperfusion injury (IRI). Furthermore, the JC-1 dye assay showed that edaravone attenuated ischemia-reperfusion-induced loss of kidney ΔΨm. CONCLUSION: Our findings indicate that EDA protects against kidney damage caused by ischemia-reperfusion through JAK/STAT signaling, inhibiting apoptosis and improving mitochondrial injury.

Minocycline promotes cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy to prevent sepsis-induced cardiac dysfunction by Akt/mTOR signaling.

Myocardial damage is responsible for the high mortality of sepsis. However, the underlying mechanism is not well understood. Cardiomyocyte autophagy alleviates the cardiac injury caused by myocardial infarction. Enhanced cardiomyocyte autophagy also has protective effects against cardiomyocyte mitochondrial injury. Minocycline enhances autophagy in many types of cells under different types of pathological stress and can be easily taken up by cardiomyocytes. The present study investigated whether minocycline prevented myocardial injury caused by sepsis and whether cardiomyocyte autophagy participated in this process. The results indicated that minocycline enhanced cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy and improved myocardial mitochondrial and cardiac function. Minocycline upregulated protein kinase B (Akt) phosphorylation, inhibited mTORC1 expression and enhanced mTORC2 expression. In conclusion, minocycline enhanced cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy and improved cardiac function. The underlying mechanisms were associated with mTORC1 inhibition and mTORC2 activation. Thus, our findings suggest that minocycline may represent a potential approach for treating myocardial injury and provide novel insights into the underlying mechanisms of myocardial injury and dysfunction after sepsis.

Ultrasound-Guided Continuous Femoral Nerve Block with Dexmedetomidine Combined with Low Concentrations of Ropivacaine for Postoperative Analgesia in Elderly Knee Arthroplasty.

OBJECTIVES: This study aims to investigate the clinical effect of dexmedetomidine (DEX) combined with low concentrations of ropivacaine in ultrasound-guided continuous fem-oral nerve block for postoperative analgesia in elderly patients with total knee arthroplasty (TKA). MATERIALS AND METHODS: Patients were divided into three groups: group C, group D1, and group D2. For postoperative analgesia, patients in group C were given 0.15% ropivacaine, patients in group D1 were given 0.15% ropivacaine + 0.02 µg × kg-1 × h-1 DEX, and patients in group D2 were given 0.15% ropivacaine + 0.05 µg × kg-1 × h-1 DEX. The visual analogue scores in the resting state, active state (AVAS), and passive functional exercise state (PVAS), degree of joint bending, and Ramsay scores were recorded. RESULTS: The Ramsay scores were significantly higher, AVAS scores were significantly lower, PVAS scores were significantly decreased, the degree of joint bending was significantly higher, and the time to the first postoperative ambulation was shorter in groups D1 and D2 than group C. Furthermore, the time to the first postoperative ambulation was shorter in group D2 than in group D1, patients in groups D1 and D2 were more satisfied than patients in group C, and patients in group D2 were more satisfied than patients in group D1. CONCLUSION: The protocol of 0.05 µg × kg-1 × h-1 of DEX combined with 0.15% ro-pivacaine in ultrasound-guided continuous femoral nerve block for postoperative analgesia in elderly patients with TKA provides a better analgesic effect than without DEX performance.X.-Y.Z. and E.-F.Z. have contributed equally to this research.

BIS-guided sedation prevents the cough reaction of patients under general anaesthesia caused by extubation: a randomized controlled trial.

BACKGROUND: The multiple modes of SARS-CoV-2 transmission including airborne, droplet, contact and faecal-oral transmissions that cause coronavirus disease 2019 (COVID-19) contribute to a public threat to the lives of people worldwide. Heavy aerosol production by coughing and the big peak expiratory flow in patients with respiratory infections (especially SARS-CoV-2) during recovery from general anaesthesia are the highest risk factors for infection in healthcare workers. To perform sedation before extubation significantly reduced the incidence of coughing during recovery from general anaesthesia. However, there are few studies on endotracheal tube removal under BIS-guided sedation in postanaesthesia care unit (PACU). We speculated that the BIS-guided sedation with dexmedetomidine and propofol would better prevent coughing caused by tracheal extubation and reducing peak expiratory flow. METHODS: Patients with general anaesthesia were randomly assigned to Group S (dexmedetomidine was infused in the operating room for 30 min, and the bispectral index (BIS) value was maintained 60-70 by infusion propofol at 0.5~1.5 µg/ml in the PACU until the endotracheal tubes were pulled out) and Group C (no dexmedetomidine and propofol treatment, replaced with the saline treatment). The incidence of coughing, agitation and active extubation, endotracheal tube tolerance and the peak expiratory flow at spontaneous breathing and at extubation were assessed. RESULTS: A total of 101 patients were randomly assigned to Group S (51 cases) and Group C (50 cases). The incidence of coughing, agitation and active extubation was significantly lower (1(51), 0(51) and 0(51), respectively) in Group S than (11(50), 8(50) and 5(50), respectively) in Group C (p < 0.05 or p < 0.01, respectively); the scores of cough were significantly reduced (1(1, 1)) in Group S than (1(1, 2)) in Group C (p < 0.01); and the endotracheal tube tolerance was significantly improved (0(0, 1)) in Group S than (1(1, 3)) in Group C (p < 0.001). The peak expiratory flow at spontaneous breathing and at extubation was significantly reduced (5(5, 7) and 6.5(6, 8), respectively) in Group S than (8(5, 10) and 21(9, 32)) in Group C (p < 0.001). CONCLUSIONS: BIS-guided sedation with dexmedetomidine and propofol significantly prevented coughing and reduced peak expiratory flow during recovery from general anaesthesia, which may play an important role in preventing medical staff from contracting COVID-19. TRIAL REGISTRATION: Chinese Clinical Trial Registry: ChiCTR2200058429 (registration date: 09-04-2022) "retrospectively registered".

Corrigendum: Interferon-induced transmembrane protein 3 in the hippocampus: a potential novel target for the therapeutic effects of recombinant human brain natriuretic peptide on sepsis-associated encephalopathy.

[This corrects the article DOI: 10.3389/fnmol.2023.1182005.].

Interferon-induced transmembrane protein 3 in the hippocampus: a potential novel target for the therapeutic effects of recombinant human brain natriuretic peptide on sepsis-associated encephalopathy.

Objective: This study aims to explore whether interferon-induced transmembrane protein 3 (IFITM3) is involved in recombinant human brain natriuretic peptide (rhBNP)-mediated effects on sepsis-induced cognitive dysfunction in mice. Methods: The cellular localization and expression level of IFITM3 in the hippocampus were detected. The IFITM3 overexpression was achieved using an intracranial stereotactic system to inject an adeno-associated virus into the hippocampal CA1 region of mice. Field experiments, an elevated plus maze, and conditioned fear memory tests assessed the cognitive impairment in rhBNP-treated septic mice. Finally, in the hippocampus of septic mice, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining and Immunoblot were used to detect changes in the protein expression of cleaved Caspase-8 and cleaved Caspase-3 in apoptosis-related pathways, and toll-like receptor 4 (TLR4) and nuclear factor κB (NF-κB) p65 in inflammatory pathways. Results: Fourteen days after cecal ligation and puncture (CLP) surgery, IFITM3 localized in the plasma membrane and cytoplasm of the astrocytes in the hippocampus of septic mice, partially attached to the perivascular and neuronal surfaces, but not expressed in the microglia. The expression of IFITM3 was increased in the astrocytes and neurons in the hippocampus of septic mice, which was selectively inhibited by the administration of rhBNP. Overexpression of IFITM3 resulted in elevated anxiety levels and long-term learning and memory dysfunction, completely abolished the therapeutic effect of rhBNP on cognitive impairment in septic mice, and induced an increase in the number of neuronal apoptosis in the hippocampal CA1 region. The expression levels of cleaved Caspase-3 and cleaved Caspase-8 proteins were significantly increased in the hippocampus, but the expression levels of TLR4 and NF-κB p65 were not increased. Conclusion: The activation of IFITM3 may be a potential new target for treating sepsis-associated encephalopathy (SAE), and it may be one of the key anti-apoptotic mechanisms in rhBNP exerting its therapeutic effect, providing new insight into the clinical treatment of SAE patients.

A subanesthetic dose of sevoflurane combined with oxygen exerts bactericidal effects and prevents lung injury through the nitric oxide pathway during sepsis.

Volatile anesthetics have been proven to treat experimental sepsis. Sevoflurane combined with oxygen is widely applied in the clinic, and our previous study indicated that this regimen significantly reduced sepsis-induced inflammatory responses and that inhibition of NF-κB pathway activation may contribute to this protection effect. Furthermore, our previous data has shown that sevoflurane combined with oxygen has prevention effect on sepsis-induced lung injury properties and bactericidal properties, but the mechanism is not well understood. Nitric oxide (NO) has been shown to have bactericidal effects and mitigating effects on lung injury, but this is not well studied in sepsis. The present study suggested that in cecal ligation and puncture (CLP)-induced sepsis, sevoflurane combined with oxygen had bactericidal effects and reduced neutrophil infiltration into the lung, preventing inflammatory lung injury. NO production was significantly induced in peritoneal lavage fluid and bronchoalveolar lavage fluid. These effects were abolished by pharmacological inhibition of nitric oxide synthase activity. Thus, our findings suggest that sevoflurane combined with oxygen exerts bactericidal effects and prevents lung injury in sepsis through the NO pathway.

Therapeutic effects of recombinant human brain natriuretic peptide on sepsis-associated encephalopathy in mice.

There is little information in the sepsis treatment guidelines on the prevention and treatment of cognitive dysfunction after sepsis. This study aimed to explore whether Recombinant human brain natriuretic peptide (rhBNP) has protective effects against sepsis-associated encephalopathy (SAE) in a mouse model. The results showed that 50 µg/kg of rhBNP significantly improved the 14-day survival of cecal ligation and puncture (CLP)-induced septic mice and mitigated cognitive dysfunction and anxiety. Fourteen days after CLP surgery, septic mice showed increased BBB permeability and neuronal apoptosis. rhBNP treatment significantly reduced pathological changes in the brain of CLP mice. Meanwhile, rhBNP therapy also reduced the level of inflammatory cytokines in the hippocampus, possibly via inhibiting the TLR4-NF-κB pathway. These results indicate that rhBNP may be a promising drug for the treatment of SAE.

Identification and structural characterisation of triterpene saponins from the root of Ardisia mamillata Hance by HPLC-ESI-QTOF-MS/MS.

Triterpene saponins in medicinal plants attract scientific attentions for their structural diversity and significant bioactivities. In this work, a high-performance liquid chromatography coupled to electrospray ionisation and quadrupole time-of-flight mass spectrometry (HPLC-ESI-QTOF-MS/MS) method is used to rapidly separate and identify triterpene saponins from the extract of Ardisia mamillata Hance (AMH). In the full scan mass spectrum, the accurate determination of molecular formula is obtained by the predominant ion [M + HCOO]- in negative ion mode. As a result, 30 triterpene saponins are identified or tentatively identified in the plant extract. Of these, 17 triterpene saponins are new compounds. In conclusion, the HPLC-ESI-QTOF-MS/MS is an efficient technique to separate and identify triterpene saponins in complex matrices of medicinal plant.

Electroacupuncture Improves Neurobehavioral Function Through Targeting of SOX2-Mediated Axonal Regeneration by MicroRNA-132 After Ischemic Stroke.

Our previous studies have shown that electroacupuncture (EA) enhances neurobehavioral functional recovery after ischemic stroke, however, the underlying regulatory mechanisms remain unclear. MicroRNAs (miRNAs) are abundant in the brain and are involved in post-transcriptional gene regulation. During cerebral ischemia reperfusion, miRNAs perform numerous biological functions in the central nervous system related to regeneration and repair of damaged nerves. Our previous studies also have shown that the expression of miRNA-132 (miR-132) is obviously down-regulated after stroke by middle cerebral artery occlusion (MCAO), which can be up-regulated by EA. This study aimed to identify whether up-regulation of miR-132 by EA improved the damaged nerves after stroke and to screen the potential target of miR-132. The results showed that EA up-regulated miR-132 thus suppressing SOX2 expression in vivo after MCAO, which obviously ameliorated neurobehavioral functional recovery. Moreover, our results also suggested that up-regulated miR-132 suppressed SOX2 in primary neurons after oxygen-glucose deprivation (OGD), which promoted neurite outgrowth. In conclusion, EA enhances neurobehavioral functional recovery against ischemic stroke through targeting of SOX2-mediated axonal regeneration by miR-132.

Combined administration of a sedative dose sevoflurane and 60% oxygen reduces inflammatory responses to sepsis in animals and in human PMBCs.

Our study aims to investigate the effects of the inhalation of subanesthestic doses of sevoflurane combined with oxygen on sepsis. Male Sprague-Dawley rats or Male ICR/Km mice underwent caecal ligation and puncture (CLP) or intraperitoneal injection of lipopolysccharide (LPS) to induce sepsis, while sham rats were used as control. Then, rats were treated with the inhalation of sevoflurane in oxygen; and air or 100% oxygen was used as control. Seven-day survival, lung injury and inflammatory factors were assessed. In this in vitro experiment, we obtained RAW264.7 macrophages and human peripheral blood mononuclear cells (PBMCs) incubated by LPS or plasma from septic patients to explore the NF-κB pathway in the effect of the inhalation of sevoflurane combined with oxygen in sepsis. In this study, we found that the inhalation of 0.5 MAC of sevoflurane in 60% oxygen was the best protocol for protecting against lethality resulting from sepsis and ALI, and there was a time window for these protective effects. We also founded that 0.5 MAC of sevoflurane in 60% oxygen inhibited the nuclear translocation of NF-κB in human PBMCs induced by LPS or plasma from septic patients. The subanesthesia dose sevoflurane in 60% oxygen may reduce sepsis-induced inflammatory responses in animals and in PBMCs, and the inhibition to the activation of the NF-κB pathway may contribute to this protection.

Sub-anesthesia Dose of Isoflurane in 60% Oxygen Reduces Inflammatory Responses in Experimental Sepsis Models.

BACKGROUND: Sepsis is a major cause of mortality in Intensive Care Units. Anesthetic dose isoflurane and 100% oxygen were proved to be beneficial in sepsis; however, their application in septic patients is limited because long-term hyperoxia may induce oxygen toxicity and anesthetic dose isoflurane has potential adverse consequences. This study was scheduled to find the optimal combination of isoflurane and oxygen in protecting experimental sepsis and its mechanisms. METHODS: The effects of combined therapy with isoflurane and oxygen on lung injury and sepsis were determined in animal models of sepsis induced by cecal ligation and puncture (CLP) or intraperitoneal injection of lipopolysaccharide (LPS) or zymosan. Mouse RAW264.7 cells or human peripheral blood mononuclear cells (PBMCs) were treated by LPS to probe mechanisms. The nuclear factor kappa B (NF-κB) signaling molecules were examined by Western blot and cellular immunohistochemistry. RESULTS: The 0.5 minimum alveolar concentration (MAC) isoflurane in 60% oxygen was the best combination of oxygen and isoflurane for reducing mortality in experimental sepsis induced by CLP, intraperitoneal injection of LPS, or zymosan. The 0.5 MAC isoflurane in 60% oxygen inhibited proinflammatory cytokines in peritoneal lavage fluids (tumor necrosis factor-alpha [TNF-ß]: 149.3 vs. 229.7 pg/ml, interleukin [IL]-1ß: 12.5 vs. 20.6 pg/ml, IL-6: 86.1 vs. 116.1 pg/ml, and high-mobility group protein 1 [HMGB1]: 323.7 vs. 449.3 ng/ml; all P< 0.05) and serum (TNF-ß: 302.7 vs. 450.7 pg/ml, IL-1ß: 51.7 vs. 96.7 pg/ml, IL-6: 390.4 vs. 722.5 pg/ml, and HMGB1: 592.2 vs. 985.4 ng/ml; all P< 0.05) in septic animals. In vitro experiments showed that the 0.5 MAC isoflurane in 60% oxygen reduced inflammatory responses in mouse RAW264.7 cells, after LPS stimulation (all P< 0.05). Suppressed activation of NF-κB pathway was also observed in mouse RAW264.7 macrophages and human PBMCs after LPS stimulation or plasma from septic patients. The 0.5 MAC isoflurane in 60% oxygen also prevented the increases of phospho-IKKß/ß, phospho-IκBß, and phospho-p65 expressions in RAW264.7 macrophages after LPS stimulation (all P< 0.05). CONCLUSION: Combined administration of a sedative dose of isoflurane with 60% oxygen improves survival of septic animals through reducing inflammatory responses.

Edaravone alleviates cell apoptosis and mitochondrial injury in ischemia-reperfusion-induced kidney injury via the JAK/STAT pathway

BACKGROUND: Kidney ischemia-reperfusion injury is a common pathophysiological phenomenon in the clinic. A large number of studies have found that the tyrosine protein kinase/signal transducer and activator of transcription (JAK/STAT) pathway is involved in the development of a variety of kidney diseases and renal protection associated with multiple drugs. Edaravone (EDA) is an effective free radical scavenger that has been used clinically for the treatment of postischemic neuronal injury. This study aimed to identify whether EDA improved kidney function in rats with ischemia-reperfusion injury by regulating the JAK/STAT pathway and clarify the underlying mechanism. METHODS: Histomorphological analysis was used to assess pathological kidney injury, and mitochondrial damage was observed by transmission electron microscopy. Terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling (TUNEL) staining was performed to detect tubular epithelial cell apoptosis. The expression of JAK2, P-JAK2, STAT3, P-STAT3, STAT1, P-STAT1, BAX and Bcl-2 was assessed by western blotting. Mitochondrial function in the kidney was assessed by mitochondrial membrane potential (ΔψM) measurement. RESULTS: The results showed that EDA inhibited the expression of p-JAK2, p-STAT3 and p-STAT1, accompanied by downregulation of the expression of Bax and caspase-3, and significantly ameliorated kidney damage caused by ischemia-reperfusion injury (IRI). Furthermore, the JC-1 dye assay showed that edaravone attenuated ischemia-reperfusion-induced loss of kidney (ΔψM). CONCLUSION: Our findings indicate that EDA protects against kidney damage caused by ischemia-reperfusion through JAK/STAT signaling, inhibiting apoptosis and improving mitochondrial injury.