Western blotting was used to detect the protein expression levels of hypoxia-inducible factor-1 (HIF-1), caspase-3, NF-κB p65, and Toll-like receptor 4 (TLR4). Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expression levels of HIF-1, NLRP3, and interleukin-1 (IL-1). Employing the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) technique, renal cell apoptosis was detected. A transmission electron microscope was used to observe the morphological alterations in renal tubular epithelial cells and mitochondria.
Compared to the control group, the ARDS model group demonstrated kidney oxidative stress and inflammatory responses, showcasing significantly elevated serum kidney injury biomarker NGAL levels, activated NF-κB/NLRP3 inflammasome signaling, increased kidney tissue cell apoptosis, and renal tubular epithelial cell damage and mitochondrial dysfunction, as visualized by transmission electron microscopy. This clearly indicates the successful induction of kidney injury in the model group. The rats given curcumin experienced a significant decrease in the injury to renal tubular epithelial cells and mitochondria, along with a notable reduction in oxidative stress, the suppression of the NF-κB/NLRP3 inflammasome pathway, and a substantial reduction in the rate of kidney tissue cell apoptosis, reflecting a dose-dependent pattern. The ARDS model group demonstrated significantly elevated levels of serum NGAL, kidney tissue MDA, and ROS, which were substantially reduced in the high-dose curcumin group (NGAL: 13817 g/L vs. 29627 g/L, MDA: 11518 nmol/g vs. 30047 nmol/g, ROS: 7519 kU/L vs. 26015 kU/L; all P < 0.05).
There was a noteworthy contrast in NLRP3 mRNA (2) expression between subjects 290039 and 949187.
Regarding IL-1 mRNA (2), a comparison of 207021 and 613132 yields noteworthy results.
A comparison of 143024 versus 395051 revealed a statistically significant difference (P < 0.05), along with a decrease in kidney tissue cell apoptosis rate from 436092% to 2775831% (P < 0.05), and a significant increase in superoxide dismutase (SOD) activity, with values of 64834 kU/g versus 43047 kU/g (P < 0.05).
In ARDS rats, curcumin's beneficial impact on kidney injury potentially stems from elevated SOD activity, reduction in oxidative stress, and inhibition of NF-κB/NLRP3 inflammasome activation.
The mechanism by which curcumin alleviates kidney injury in ARDS rats may include boosting SOD activity, decreasing oxidative stress, and inhibiting the activation of the NF-κB/NLRP3 inflammasome.
To explore the incidence and predisposing factors of hypothermia in individuals with acute renal injury (AKI) undergoing continuous renal replacement therapy (CRRT), and to compare the effectiveness of varied heating techniques in managing hypothermia in CRRT patients.
A prospective investigation into the matter was initiated. Subjects enrolled in this study were AKI patients undergoing continuous renal replacement therapy (CRRT) at the Department of Critical Care Medicine, First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), spanning from January 2020 to December 2022. By way of a randomized numerical table, patients were grouped, specifically into a dialysate heating group and a reverse-piped heating group. The bedside physician provided both groups with treatment modalities and settings that were appropriate, considering the specific condition of each patient. The AsahiKASEI dialysis machine's heating panel was utilized by the dialysis heating group to heat the dialysis solution to a temperature of 37 degrees Celsius. For heating the dialysis solution, the reverse-piped heating group of the Prismaflex CRRT system utilized the Barkey blood heater, set to 41 degrees Celsius. The patient's temperature was then the focus of continuous monitoring efforts. Hypothermia occurs when the body temperature falls below 36 degrees Celsius or declines by more than one degree Celsius from the person's resting temperature. The incidence and persistence of hypothermia were analyzed across both groups, to determine any differences. The research employed binary multivariate logistic regression analysis to explore the association between hypothermia and various factors in patients with acute kidney injury undergoing continuous renal replacement therapy (CRRT).
Including 37 patients in the dialysate heating group and 36 in the reverse-piped heating group, a total of 73 patients with AKI treated with CRRT were enrolled in the study. Hypothermia was significantly less frequent in the dialysis heating group than in the reverse-piped heating group (15 cases out of 37 in the dialysis group versus 25 cases out of 36 in the reverse-piped group; 405% vs. 694%, P < 0.005), and hypothermic onset was delayed in the dialysis heating group, occurring at 540092 hours compared to 335092 hours in the reverse-piped group (P < 0.001). Patients were divided into groups, hypothermic and non-hypothermic, based on the presence or absence of hypothermia. A univariate analysis of all measured parameters revealed a substantial decrease in mean arterial pressure (MAP) in hypothermic patients (n = 40) when compared to non-hypothermic patients (n = 33), a statistically significant difference (P < 0.001). MAP values were 77451247 mmHg (1 mmHg = 0.133 kPa) for hypothermic patients and 94421451 mmHg for non-hypothermic patients, suggesting shock and the administration of medium and high doses of vasoactive drugs (0.2-0.5 g/kg).
min
More than 0.5 grams per kilogram of a high dose is given.
min
The treatment group experienced an exceptional 825% (33 of 40) increase in the administration of medium and high doses of vasoactive drugs compared to the control group's increase of 182% (6 out of 33).
h
Regarding the comparison of 5150938 and 38421097, there were statistically significant differences (P < 0.05) evident. The CRRT heating methods further highlighted these differences. Specifically, the hypothermia group predominantly used infusion line heating (625% – 25 cases out of 40 total), while the non-hypothermia group relied primarily on dialysate heating (667% – 22 cases out of 33 total), exhibiting a statistically significant difference (P < 0.05). In a binary multivariate Logistic regression analysis, shock (odds ratio [OR] = 17633, 95% confidence interval [95%CI] 1487-209064), mid-to-high-dose vasoactive drug administration (OR = 24320, 95%CI 3076-192294), CRRT heating type (reverse-piped; OR = 13316, 95%CI 1485-119377), and CRRT treatment dose (OR = 1130, 95%CI 1020-1251) were associated with hypothermia in AKI patients undergoing CRRT (all p < 0.005), whereas MAP acted as a protective factor (OR = 0.922, 95%CI 0.861-0.987, p < 0.005).
Continuous renal replacement therapy (CRRT) for acute kidney injury (AKI) patients frequently leads to hypothermia, but using heated CRRT fluids can effectively diminish its prevalence. The use of continuous renal replacement therapy (CRRT) in acute kidney injury (AKI) patients is associated with several factors that increase the risk of hypothermia: shock, medium and high dosages of vasoactive drugs, CRRT heating methods, and treatment dose. Mean arterial pressure (MAP), in contrast, seems to be a protective factor in this context.
A common adverse effect for AKI patients during CRRT is hypothermia, and this problem can be reduced by using heated CRRT fluids. Hypothermia during CRRT in patients with acute kidney injury (AKI) is associated with factors including medium and high vasoactive drug dosages, the CRRT heating method used, and the treatment dose. Mean arterial pressure (MAP) exhibits a protective association.
To determine the effect of the phosphate and tension homology (PTEN) and its impact on PINK1/Parkin pathway activation in relation to hippocampal mitophagy and cognitive function in a mouse model of sepsis-associated encephalopathy (SAE), and understanding the associated mechanisms.
Random assignment of 80 male C57BL/6J mice resulted in five groups of 16 mice each: Sham, cecal ligation puncture (CLP), PINK1 plasmid transfection pretreatment groups (p-PINK1+Sham, p-PINK1+CLP), and empty vector plasmid transfection control (p-vector+CLP). CLP-treated mice in the experimental groups were used to create SAE models. 2′-C-Methylcytidine concentration Merely laparotomy was executed on the mice of the Sham groups. Animals in the p-PINK1+Sham and p-PINK1+CLP groups received PINK1 plasmid transfection via the lateral ventricle, 24 hours prior to surgery; conversely, animals in the p-vector+CLP group received the empty vector plasmid. The Morris water maze experiment was finalized 7 days after the CLP. Upon collecting hippocampal tissues, pathological modifications were observed microscopically under a light microscope after hematoxylin-eosin (HE) staining. Further analysis involved observation of mitochondrial autophagy using transmission electron microscopy following uranyl acetate and lead citrate staining. Analysis by Western blotting revealed the expressions of PINK1, Parkin, Beclin1, interleukins (IL-6, IL-1) and microtubule-associated protein 1 light chain 3 (LC3).
CLP group mice, when measured against the Sham group in the Morris water maze task, displayed an increased escape latency, a decreased time spent in the target quadrant, and a reduced count of platform crossings across the first four days. In the mouse's hippocampus, as observed under the light microscope, the structure was injured, exhibiting disordered neuronal cell arrangement, and pyknotic nuclei. Anteromedial bundle With the use of an electron microscope, swollen, round mitochondria were identified, exhibiting bilayer or multilayer membrane wrappers. host-microbiome interactions The CLP group, in comparison to the Sham group, demonstrated heightened expression levels of PINK1, Parkin, Beclin1, LC3II/LC3I ratio, IL-6, and IL-1 in the hippocampus. This implies that CLP-induced sepsis activated inflammatory pathways and stimulated PINK1/Parkin-mediated mitophagy. As opposed to the CLP group, the p-PINK1+CLP group experienced faster escape latencies, increased time spent in, and more crossings within the target quadrant between days 1 and 4. Under the light microscope, the mouse hippocampal structures underwent destruction, presenting with disorderly neuron arrangements and pyknotic nuclei.