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Representative western blot analysis of β-arrestin 2 protein in liver (a), lung (b), and kidney (c) from animals subjected to CLP followed by LT or LS procedures and naïve animals. Data represent the mean ± SD of seven animals. P*<0.05 compared with naïve; P#<0.05 compared with LT.
Source publication
Laparoscopy (LS) has been shown to decrease the inflammatory sequelae of endotoxemia. β-arrestin 2 plays an important function in signal transduction pathway of TLR4. High mobility group box-1 (HMGB-1) is involved in the delayed systemic inflammatory response. We investigated the effects of CO2 insufflation on liver, lung, and kidney expression of...
Citations
... The results of an experimental study on a murine NB model show an increase in liver metastases after pneumoperitoneum with CO 2 , while local peritoneal carcinosis does not seem to increase. Therefore, it remains to be determined whether this is due to local immune suppression or direct modulation of tumor cell behaviour [11][12][13]. ...
Purpose
The proto-oncogene MYCN is considered a transcription factor involved in the regulation of neuroblastoma (NB) cell biology. Since minimally invasive-surgery represents a debated treatment of NB, we investigated CO2 effects on proliferative activity and apoptotic pathway in two NB cell lines, SH-SY5Y (MYCN-non-amplified) and IMR-32 (MYCN-amplified).
Methods
SH-SY5Y and IMR-32 were exposed to CO2 (100%) at a pressure of 15 mmHg for 4 h and then moved to normal condition for 24 h. Cell proliferation, caspase 3 activity and transcript levels of BAX, BCL-2, cyclin B, cyclin D and MMP-2 were evaluated.
Results
CO2 exposure caused a decrease in cell proliferation associated to increases in BAX/BCL-2 ratio and caspase 3 activity in SH-SY5Y, while opposite effects have been found in IMR-32. CO2 exposure induced a decrease of cyclin B1 in SH-SY5Y, while an increase in cyclin B1 and D1 was observed in IMR-32. A slight up-regulation of MMP-2 expression in SH-SY5Y and a significant increase of 2.2 folds in IMR-32 was observed (p < 0.05).
Conclusions
Our results suggest that CO2 exposure may cause different effects on various NB cell lines, likely due to MYCN amplification status. Further in vitro and in vivo studies are needed to highlight the role of laparoscopy on NB behaviour.
... According to the relevant literature and the results of preliminary experiments, we developed a mouse model of pneumoperitoneum-induced lung injury [13,46,47]. After insufflation (1 h) and deflation (3 h) with CO 2 , we found leukocyte infiltration and visible alveolar structure damage in lung tissues by histological examination, which suggested the successful establishment of the mouse model [38,48]. ...
Various pharmacological agents and protective methods have been shown to reverse pneumoperitoneum-related lung injury, but identifying the best strategy is challenging. Herein, we employed lung tissues and blood samples from C57BL/6 mice with pneumoperitoneum-induced lung injury and blood samples from patients who received laparoscopic gynecological surgery to investigate the therapeutic role of hydromorphone in pneumoperitoneum-induced lung injury along with the underlying mechanism. We found that pretreatment with hydromorphone alleviated lung injury in mice that underwent CO2 insufflation, decreased the levels of myeloperoxidase (MPO), total oxidant status (TOS), and oxidative stress index (OSI), and increased total antioxidant status (TAS). In addition, after pretreatment with hydromorphone, upregulated HO-1 protein expression, reduced mitochondrial DNA content, and improved mitochondrial morphology and dynamics were observed in mice subjected to pneumoperitoneum. Immunohistochemical staining also verified that hydromorphone could increase the expression of HO-1 in lung tissues in mice subjected to CO2 pneumoperitoneum. Notably, in mice treated with HO-1-siRNA, the protective effects of hydromorphone against pneumoperitoneum-induced lung injury were abolished, and hydromorphone did not have additional protective effects on mitochondria. Additionally, in clinical patients who received laparoscopic gynecological surgery, pretreatment with hydromorphone resulted in lower serum levels of club cell secretory protein-16 (CC-16) and intercellular adhesion molecule-1 (ICAM-1), a lower prooxidant-antioxidant balance (PAB), and higher heme oxygenase-1 (HO-1) activity than morphine pretreatment. Collectively, our results suggest that hydromorphone protects against CO2 pneumoperitoneum-induced lung injury via HO-1-regulated mitochondrial dynamics and may be a promising strategy to treat CO2 pneumoperitoneum-induced lung injury.
... Estudios más recientes con medición de marcadores más específicos de inflamación e inmunidad, han demostrado que el neumoperitoneo con CO 2 disminuye la carga bacteriana del peritoneo, eleva la expresión de β arrestina 2, bloquea la expresión de HMGB 1 (high mobility group box 1) (ambos reguladores de inflamación y sistemas inmunológicos) y reduce la expresión de mieloperoxidasa en el hígado, pulmón y riñones, reflejando un efecto aparentemente protector del neumoperitoneo en los animales. 37 También se ha descrito efecto protector y mejor modulación de la respuesta inmunológica en ratas sometidas a neumoperitoneo con CO 2 , comparado contra helio o laparotomía. 34 Otro estudio encontró que el neumoperitoneo provocó menor respuesta inflamatoria y menor afectación al sistema inmunológico, así como más rápida recuperación de los animales. ...
... 27 However, other studies presenting different opinions noted that the incidence rate of BT under CDP was not significantly higher than that under laparotomy for the animal models with intra- abdominal infection. 28 Moreover, there was no signifi- cant difference in the incidence rate of bacteremia, endotoxemia, and clinical sepsis between CDP and laparotomy. 29,30 Findings of This study ...
Objective:
To explore the influence of carbon dioxide pneumoperitoneum (CDP) on system inflammatory response syndrome (SIRS) and bacterial translocation (BT) in patients with bacterial peritonitis (BP) caused by acute appendicitis (AA).
Methods:
Eighty-six consecutive subjects were randomly divided into the laparoscopy and laparotomy groups (n = 44 and n = 42, respectively). The levels of white blood cells (WBC), C-reactive protein (CRP), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) of the 2 groups were tested preoperatively and at days 1, 2, and 4 after surgery. Blood and secretion culture was performed to verify whether septicemia or incision infection occurred, respectively. And the abdominal ultrasound or computed tomography scanning was used to diagnose peritoneal abscess for the suspected patients. The essential risk factors related to the aggravation of SIRS were analyzed through analysis of variance and binary logistic regression.
Results:
The postoperative blood levels of WBC, CRP, TNF-α, and IL-6 on day 4 in the laparoscopy group were significantly lower than those in the control group (all Ps < .05). The differences in incidence rates of septicemia and peritoneal abscess between the CDP and control groups were not statistically significant ( P > .05). Nevertheless, the incision infection rate in the laparoscopy group was apparently lower than that in the control group (4.55% vs 19.04%, P = .047). Analysis of variance and binary logistic regression showed that the non-pneumoperitoneum, pathological type of appendicitis, and multidrug resistant infections were the 3 major risk factors for SIRS (the P values were .001, .019, and .012, respectively).
Conclusion:
It was found that CDP is safe for BP and could be a potential protective factor to mitigate BP effectively, indicating that the performance of laparoscopy operation under CDP is feasible to control SIRS; at the same time, CDP would not raise the incidence rate of BT.
High mobility group box 1 (HMGB1) is a highly conserved nucleoprotein involving in numerous biological processes, and well known to trigger immune responses as the damage-associated molecular pattern (DAMP) in the extracellular environment. The role of HMGB1 is distinct due to its multiple functions in different subcellular location. In the nucleus, HMGB1 acts as a chaperone to regulate DNA events including DNA replication, repair and nucleosome stability. While in the cytoplasm, it is engaged in regulating autophagy and apoptosis. A great deal of research has explored its function in the pathogenesis of renal diseases. This review mainly focuses on the role of HMGB1 and summarizes the pathway and treatment targeting HMGB1 in the various renal diseases which may open the windows of opportunities for the development of desirable therapeutic ends in these pathological conditions.
As yet, there was no effective pharmacological therapy approved for non‐alcoholic fatty liver disease (NAFLD). Here, we aimed to evaluate the therapeutic potential of puerarin against NAFLD and explored the underlying mechanisms. C57BL/6J mice were fed with a high‐fat high‐sucrose (HFHS) diet with or without puerarin coadministration intragastrically. The levels of hepatocellular injury, steatosis, fibrosis, and mitochondrial and metabolism alteration were detected. First, puerarin ameliorated histopathologic abnormalities due to HFHS. We observed a marked increase in hepatic lipid content, inflammation, and fibrosis level, which were attenuated by puerarin. Possible mechanisms were related to puerarin‐mediated activation of PI3K/AKT pathway and further improvement in fatty acid metabolism. Puerarin restored the NAD+ content and beneficially affected the hepatic mitochondrial function, which attenuated HFHS‐induced steatosis and metabolic disturbances. Finally, hepatic PARP‐1 was activated due to excessive fat intake. Puerarin attenuated the PARP‐1 expression in HFHS‐fed mice, and PJ34, the PARP inhibitor, could mimic these protections of puerarin. However, pharmacological inhibition of PI3K disabled the protection of puerarin or PJ34 toward NAD+ refilling and mitochondrial homeostasis. In conclusion, our findings indicated that puerarin could be a promising and practical therapeutic strategy in NAFLD through modulating PARP‐1/PI3K/AKT signaling pathway and further facilitating mitochondrial function.
