The protein expression of hypoxia-inducible factor-1 (HIF-1), caspase-3, NF-κB p65, and Toll-like receptor 4 (TLR4) was measured via the Western blot technique. Reverse transcription-polymerase chain reaction (RT-PCR) techniques were employed to ascertain the mRNA expressions of HIF-1, NLRP3, and interleukin-1 (IL-1). Renal cell apoptosis was measured via the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) technique. Under a transmission electron microscope, the morphological changes in renal tubular epithelial cells and mitochondria were examined.
The ARDS model's kidney injury was confirmed by the presence of oxidative stress and inflammatory responses, which translated to significant serum NGAL increases. Further confirming the injury was the activation of NF-κB/NLRP3 inflammasome pathways, kidney tissue apoptosis, and observed damage to renal tubular epithelial cells and mitochondria—all visualized via transmission electron microscopy—demonstrating the model's successful induction of kidney injury. Following curcumin treatment, a considerable reduction in renal tubular epithelial cell and mitochondrial damage was observed in the rats, coupled with a notable decrease in oxidative stress, a blockage of the NF-κB/NLRP3 inflammasome pathway, and a significant decline in kidney tissue apoptosis, exhibiting a clear dose-dependent response. The high-dose curcumin group demonstrated significantly lower serum NGAL, kidney tissue MDA, and ROS levels than the ARDS model 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), a clear indication of curcumin's impact.
The NLRP3 mRNA levels were examined in two groups, 290039 and 949187, revealing contrasting results.
When evaluating 207021 and 613132, the IL-1 mRNA (2) measurement demonstrates a variation.
In a comparative study, 143024 and 395051 exhibited significant differences (P < 0.05), accompanied by a noteworthy decrease in kidney tissue cell apoptosis rate (436092% vs. 2775831%, P < 0.05) and a substantial increase in SOD activity (64834 kU/g vs. 43047 kU/g) (P < 0.05).
A potential mechanism for curcumin's ability to ameliorate kidney injury in ARDS rats may be related to the elevation of SOD activity, decreased oxidative stress, and the inhibition of NF-κB/NLRP3 inflammasome signaling.
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 longitudinal observational study was conducted. The research sample comprised patients with acute kidney injury (AKI) undergoing continuous renal replacement therapy (CRRT) at the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital)'s Department of Critical Care Medicine, admitted between January 2020 and December 2022. Patients were stratified into a dialysate heating group and a reverse-piped heating group using a randomized numerical table as the allocation method. In accordance with each patient's specific condition, the bedside physician established suitable treatment methods and parameters for both groups. Using the AsahiKASEI dialysis machine's heating panel, the dialysis heating team raised the dialysis solution's temperature to 37 degrees Celsius. Using the Barkey blood heater within the Prismaflex CRRT system's reverse-piped heating group, the dialysis solution's temperature was maintained at 41 degrees Celsius. Thereafter, the patient's temperature was continuously tracked. A person is deemed to have hypothermia if their body temperature is below 36 degrees Celsius or decreases by over 1 degree Celsius from their initial body temperature. Comparing the two groups, a study evaluated the frequency and duration of hypothermia episodes. A multivariate logistic regression analysis, specifically a binary model, was utilized to examine the variables associated with hypothermia during continuous renal replacement therapy (CRRT) in patients with acute kidney injury (AKI).
Following treatment with CRRT, a total of 73 AKI patients were enrolled; 37 in the dialysate heating group and 36 in the reverse-piped heating group. A significantly lower rate of hypothermia was observed in the dialysis heating group compared to the reverse-piped heating group (405% [15/37] versus 694% [25/36], P < 0.005). Furthermore, hypothermia presented later in the dialysis heating group (540092 hours) than in the reverse-piped heating group (335092 hours), with a statistically significant difference (P < 0.001). Hypothermic and non-hypothermic patient groups were established based on the presence or absence of hypothermia. Analysis of all indicators demonstrated a statistically significant drop in mean arterial pressure (MAP) for hypothermic patients (n = 40) versus non-hypothermic patients (n = 33). This difference was statistically significant (P < 0.001), with MAP readings of 77451247 mmHg (1 mmHg = 0.133 kPa) in hypothermic patients and 94421451 mmHg in non-hypothermic patients, indicative of shock, and the administration of medium and high doses of vasoactive drugs (0.2-0.5 g/kg).
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Greater than 0.5 grams per kilogram high dose is commonly prescribed.
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Administration of Continuous Renal Replacement Therapy (CRRT) treatment demonstrated a dramatic increase in the treatment group, with 450% (18 of 40) of patients receiving it versus 61% (2 of 33) in the control group.
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Analysis of 5150938 and 38421097 revealed significant differences (P < 0.05) in CRRT heating types. The hypothermia group displayed a strong preference for infusion line heating, comprising 625% of cases (25 out of 40), in contrast to the non-hypothermia group, where dialysate heating was the main method (667%, 22 of 33). This difference also demonstrated statistical significance (P < 0.05). A binary multivariate Logistic regression analysis, incorporating the aforementioned indicators, revealed shock as a risk factor (odds ratio [OR] = 17633, 95% confidence interval [95%CI] 1487-209064), along with mid-to-high-dose vasoactive drugs (OR = 24320, 95%CI 3076-192294), reverse-piped CRRT heating (OR = 13316, 95%CI 1485-119377), and CRRT treatment dose (OR = 1130, 95%CI 1020-1251) for hypothermia in AKI patients undergoing CRRT (all p < 0.005). Conversely, MAP proved a protective factor (OR = 0.922, 95%CI 0.861-0.987, p < 0.005).
Acute kidney injury (AKI) patients undergoing continuous renal replacement therapy (CRRT) frequently experience hypothermia, a condition whose prevalence can be lowered by heating the CRRT treatment fluids. Hypothermia during continuous renal replacement therapy (CRRT) in acute kidney injury (AKI) patients is potentially influenced by shock, medium and high doses of vasoactive medications, variations in CRRT heating methods, and the quantity of CRRT treatment. Mean arterial pressure (MAP) exhibits a protective role against this risk.
A common adverse effect for AKI patients during CRRT is hypothermia, and this problem can be reduced by using heated CRRT fluids. High or medium doses of vasoactive medications, the type of heating used during CRRT, and the prescribed CRRT dose itself, all serve as risk factors for hypothermia in patients with acute kidney injury (AKI) undergoing CRRT. Mean arterial pressure (MAP) is, however, a protective factor.
A study examining the potential consequences of the PTEN-induced kinase 1 (PINK1)/Parkin pathway on hippocampal mitophagy and cognitive function in mice affected by sepsis-associated encephalopathy (SAE), and a possible elucidation of its underlying mechanism.
Eight groups of 16 male C57BL/6J mice each were randomly assigned from a pool of 80 male C57BL/6J mice to the following conditions: Sham, cecal ligation puncture (CLP), PINK1 plasmid transfection pretreatment (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. Roxadustat In the Sham groups, the mice had laparotomy as the sole surgical intervention. The p-PINK1+Sham and p-PINK1+CLP groups of animals received PINK1 plasmid transfection through the lateral ventricle 24 hours before the operation, while mice in the p-vector+CLP group received a control empty plasmid. The Morris water maze experiment took place 7 days following the CLP intervention. A light microscopic examination, post-hematoxylin-eosin (HE) staining, of the collected hippocampal tissues revealed the pathological changes, followed by the observation of mitochondrial autophagy under transmission electron microscopy employing uranyl acetate and lead citrate staining. Western blotting confirmed the expression levels of PINK1, Parkin, Beclin1, interleukins (IL-6, IL-1), and microtubule-associated protein 1 light chain 3 (LC3).
Compared with the Sham group, CLP group mice in the Morris water maze test demonstrated a more drawn-out escape latency, a reduced amount of time spent in the target quadrant, and a diminished number of platform crossings between days 1 and 4. Under the scrutinizing gaze of the light microscope, the mouse's hippocampal structure bore the scars of injury, its neuronal cells exhibiting a chaotic arrangement, and its nuclei displaying pyknosis. biopsy naïve Electron microscopy showed mitochondria to be swollen, round, and enveloped by bilayer or multilayer membrane structures. biopsy site identification CLP group hippocampal expression of PINK1, Parkin, Beclin1, LC3II/LC3I ratio, IL-6, and IL-1 exceeded that of the Sham group, hinting that CLP-induced sepsis fostered an inflammatory response and led to the activation of PINK1/Parkin-mediated mitophagy. Escape latencies were shorter and time within the target quadrant and crossings within it were more frequent in the p-PINK1+CLP group compared with the CLP group over the 1 to 4 day timeframe. Disorderly neuron arrangements and pyknotic nuclei were found in the destroyed hippocampal structures of mice, as observed under the light microscope.