[Curcumin alleviates nuclear factor-κB/NOD-like receptor protein 3 mediated renal injury caused by acute respiratory distress syndrome through reducing mitochondrial oxidative stress].

OBJECTIVE: To evaluate the effect of curcumin on renal mitochondrial oxidative stress, nuclear factor-κB/NOD-like receptor protein 3 (NF-κB/NLRP3) inflammatory body signaling pathway and tissue cell injury in rats with acute respiratory distress syndrome (ARDS). METHODS: A total of 24 specific pathogen free (SPF)-grade healthy male Sprague-Dawley (SD) rats were randomly divided into control group, ARDS model group, and low-dose and high-dose curcumin groups, with 6 rats in each group. The ARDS rat model was reproduced by intratracheal administration of lipopolysaccharide (LPS) at 4 mg/kg via aerosol inhalation. The control group was given 2 mL/kg of normal saline. The low-dose and high-dose curcumin groups were administered 100 mg/kg or 200 mg/kg curcumin by gavage 24 hours after model reproduction, once a day. The control group and ARDS model group were given an equivalent amount of normal saline. After 7 days, blood samples were collected from the inferior vena cava, and the levels of neutrophil gelatinase-associated lipocalin (NGAL) in serum were determined by enzyme-linked immunosorbent assay (ELISA). The rats were sacrificed, and kidney tissues were collected. Reactive oxygen species (ROS) levels were determined by ELISA, superoxide dismutase (SOD) activity was detected using the xanthine oxidase method, and malondialdehyde (MDA) levels were determined by colorimetric method. The protein expressions of hypoxia-inducible factor-1α (HIF-1α), caspase-3, NF-κB p65, and Toll-like receptor 4 (TLR4) were detected by Western blotting. The mRNA expressions of HIF-1α, NLRP3, and interleukin-1ß (IL-1ß) were detected by reverse transcription-polymerase chain reaction (RT-PCR). Renal cell apoptosis was detected by TdT-mediated dUTP nick end labeling (TUNEL). The morphological changes in renal tubular epithelial cells and mitochondria were observed under a transmission electron microscope. RESULTS: Compared with the control group, the ARDS model group exhibited kidney oxidative stress and inflammatory response, significantly elevated serum levels of kidney injury biomarker NGAL, activated NF-κB/NLRP3 inflammasome signaling pathway, increased kidney tissue cell apoptosis rate, and renal tubular epithelial cell damage and mitochondrial integrity destruction under transmission electron microscopy, indicating successful induction of kidney injury. Following curcumin intervention, the injury to renal tubular epithelial cells and mitochondria in the rats was significantly mitigated, along with a noticeable reduction in oxidative stress, inhibition of the NF-κB/NLRP3 inflammasome signaling pathway, and a significant decrease in kidney tissue cell apoptosis rate, demonstrating a certain dose-dependency. Compared with the ARDS model group, the high-dose curcumin group exhibited significantly reduced serum NGAL levels and kidney tissue MDA and ROS levels [NGAL (µg/L): 13.8±1.7 vs. 29.6±2.7, MDA (nmol/g): 115±18 vs. 300±47, ROS (kU/L): 75±19 vs. 260±15, all P < 0.05], significantly down-regulated protein expressions of HIF-1α, caspase-3, NF-κB p65, and TLR4 in the kidney tissue [HIF-1α protein (HIF-1α/ß-actin): 0.515±0.064 vs. 0.888±0.055, caspase-3 protein (caspase-3/ß-actin): 0.549±0.105 vs. 0.958±0.054, NF-κB p65 protein (NF-κB p65/ß-actin): 0.428±0.166 vs. 0.900±0.059, TLR4 protein (TLR4/ß-actin): 0.683±0.048 vs. 1.093±0.097, all P < 0.05], and significantly down-regulated mRNA expressions of HIF-1α, NLRP3, and IL-1ß [HIF-1α mRNA (2-ΔΔCt): 2.90±0.39 vs. 9.49±1.87, NLRP3 mRNA (2-ΔΔCt): 2.07±0.21 vs. 6.13±1.32, IL-1ß mRNA (2-ΔΔCt): 1.43±0.24 vs. 3.95±0.51, all P < 0.05], and significantly decreased kidney tissue cell apoptosis rate [(4.36±0.92)% vs. (27.75±8.31)%, P < 0.05], and significantly increased SOD activity (kU/g: 648±34 vs. 430±47, P < 0.05). CONCLUSIONS: Curcumin can alleviate kidney injury in ARDS rats, and its mechanism may be related to the increasing in SOD activity, reduction of oxidative stress, and inhibition of the activation of the NF-κB/NLRP3 inflammasome signaling pathway.

Survival of a patient who received extracorporeal membrane oxygenation due to postoperative myocardial infarction: A case report.

BACKGROUND: Cardiac arrest after noncardiac surgery is a dangerous complication that may contribute to mortality. Because of the high mortality rate and many complications of cardiac arrest, it is very important to identify and correct a reversible etiology early. By reporting the treatment process of this case, we aimed to broaden the diagnosis and treatment of cardiac arrest after noncardiac surgery and describe how cardiopulmonary resuscitation using extracorporeal membrane oxygenation (ECMO) can improve a patient's chance of survival. CASE SUMMARY: A 69-year-old man visited our hospital complaining of low back pain on July 12, 2021. Magnetic resonance imaging showed lumbar disc herniation. Two hours after lumbar disc herniation surgery, the patient developed cardiac arrest. Cardiopulmonary resuscitation was performed, and ECMO was started 60 min after the initiation of cardiopulmonary resuscitation. Regarding the etiology of early cardiac arrest after surgery, acute myocardial infarction and pulmonary embolism were considered first. Based on ultrasound evaluation, acute myocardial infarction appeared more likely. Coronary angiography confirmed occlusion of the left anterior descending branch, and coronary artery stenting was performed. Pulmonary artery angiography was performed to exclude pulmonary embolism. Due to heparinization during ECMO and coronary angiography, there was a large amount of oozing blood in the surgical incision. Therefore, heparin-free ECMO was performed in the early stage, and routine heparinized ECMO was performed after hemorrhage stabilization. Eventually, the patient was discharged and made a full neurologic recovery. CONCLUSION: For early postoperative cardiac arrest, acute myocardial infarction should be considered first, and heparin should be used with caution.

Helium-neon laser therapy in the treatment of hydroxyapatite orbital implant exposure: A superior option.

The aim of the present study was to evaluate the efficacy of helium-neon laser therapy in the treatment of hydroxyapatite orbital implant exposure and compare the results with those of a combined drugs and surgery regimen. A total of 70 patients with hydroxyapatite orbital implant exposure in 70 eyes were randomly divided into two groups: Helium-neon laser therapy (group A) and drugs plus surgery (group B). Each group contained 35 patients. The healing rates and times of the conjunctival wound were recorded and compared following helium-neon laser treatment or the drugs plus surgery regimen. Changes in the hydroxyapatite orbital implant prior to and following helium-neon laser irradiation were analyzed. A similar animal study was conducted using 24 New Zealand white rabbits, which received orbital implants and were then received drug treatment or helium-neon therapy. In the human experiment, the rates for conjunctival wound healing were 97.14% in group A and 74.29% in group B, with a significant difference between the groups (χ2=5.71, P<0.05). Patients with mild exposure were healed after 7.22±2.11 days of helium-neon laser therapy and 14.33±3.20 days of drugs plus surgery. A statistically significant difference was found between the groups (t=8.97, P<0.05). Patients with moderate to severe exposure were healed after 18.19±2.12 days of helium-neon laser therapy and 31.25±4.21 days of drugs plus surgery. The difference between the groups was statistically significant (t=7.91, P<0.05). Enhanced magnetic resonance imaging showed that the helium-neon laser therapy significantly promoted vascularization of the hydroxyapatite orbital implant. These results, combined with pathological findings in animals, which showed that a helium-neon laser promoted vascularization and had anti-inflammatory effects, suggest that helium-neon laser irradiation is an effective method for treating hydroxyapatite orbital implant exposure, thereby avoiding secondary surgery.