Dataset Information

Protective effects of postconditioning in transvaginally created pneumoperitoneum.

ABSTRACT: There are reports of ischemic complications in clinical practice after laparoscopy using pneumoperitoneum. Conditioning has a beneficial effect for various ischemic diseases. This experimental study was designed to evaluate the effects of postconditioning in transvaginally created pneumoperitoneum. Sixty adult female rats, weighing 300±50 g were divided into four equal groups. Pneumoperitoneum was created by CO2 insufflation under a pressure of 10 mmHg. Rats in the first group (sham) were subjected to only sham-operation or gas insufflation. The second group (TV/PP) was subjected to pneumoperitoneum for 60 min followed by 30 min of desufflation. The third group (post-5) was subjected to pneumoperitoneum for 60 min followed by 5 min of desufflation, 5 min of insufflation and again followed by 30 min of desufflation. The fourth group (post-2.5) was subjected to pneumoperitoneum for 60 min followed by 2.5 min of desufflation and 2.5 min of insufflation-repeated in two cycles- and then followed by 30 min of desufflation. The rats were sacrificed, and blood was collected after 30 min, 2 and 6 h from the last desufflation. Levels of oxidative stress markers, malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH), sulfhydryl groups (SH) and inflammatory cytokine TNF-α, were analyzed. Levels of MDA in the post-5 group were significantly reduced compared to the TV/PP and post-2.5 groups. The level of GSH in TV/PP animals was markedly reduced compared to the Sham, Post-5 and Post-2.5 groups. In addition, levels of SH were increased in the Post-5 group in comparison to the Sham, TV/PP and Post-2.5 groups. No difference in the activity of SOD between the groups was found, and the concentration of TNF-α in TV/PP animals was significantly higher than that in the Sham and postconditioning groups. Overall, the results of the present study indicate that postconditioning can reduce pneumoperitoneum-induced oxidative injury.

SUBMITTER: Shanava K

PROVIDER: S-EPMC7185089 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Protective effects of postconditioning in transvaginally created pneumoperitoneum.

Shanava Koba K Javor Szaniszlo S Kerkadze Vakhtang V Abiatari Ivane I Weber György G

Experimental and therapeutic medicine 20200319 6

There are reports of ischemic complications in clinical practice after laparoscopy using pneumoperitoneum. Conditioning has a beneficial effect for various ischemic diseases. This experimental study was designed to evaluate the effects of postconditioning in transvaginally created pneumoperitoneum. Sixty adult female rats, weighing 300±50 g were divided into four equal groups. Pneumoperitoneum was created by CO<sub>2</sub> insufflation under a pressure of 10 mmHg. Rats in the first group (sham) ...[more]

PMID: 32346452

Similar Datasets

Project description:BackgroundSevoflurane postconditioning (SevP) effectively relieves myocardial ischemia/reperfusion (I/R) injury but performs poorly in the diabetic myocardium. Previous studies have revealed the important role of increased oxidative stress in diabetic tissues. Notably, mitochondrial fission mediated by dynamin-related protein 1 (Drp1) is an upstream pathway of reactive oxygen production. Whether the ineffectiveness of SevP in the diabetic myocardium is related to Drp1-dependent mitochondrial fission remains unknown. This study aimed to explore the important role of Drp1 in the diabetic myocardium and investigate whether Drp1 inhibition could restore the cardioprotective effect of SevP.MethodsIn the first part of the study, adult male Sprague-Dawley rats were divided into 6 groups. Rats in the diabetic groups were fed with high-fat and high-sugar diets for 8 weeks and injected intraperitoneally with streptozotocin (35 mg/kg). Myocardial I/R was induced by 30 min of occlusion of the left anterior descending branch of the coronary artery followed by 120 min of reperfusion. SevP was applied by continuous inhalation of 2.5 % sevoflurane 1 min before reperfusion, which lasted for 10 min. In the second part of the study, we applied mdivi-1 to investigate whether Drp1 inhibition could restore the cardioprotective effect of SevP in the diabetic myocardium. The myocardial infarct size, mitochondrial ultrastructure, apoptosis index, SOD activity, MDA content, and Drp1 expression were detected.ResultsTTC staining and TUNEL results showed that the myocardial infarct size and apoptosis index were increased in the diabetic myocardium. However, SevP significantly alleviated myocardial I/R injury in the normal myocardium but not in the diabetic myocardium. Additionally, we found an elevation in Drp1 expression, accompanied by more severe fission-induced structural damage and oxidative stress in the diabetic myocardium. Interestingly, we discovered that the beneficial effect of SevP was restored by mdivi-1, which significantly suppressed mitochondrial fission and oxidative stress.ConclusionsOur study demonstrates the crucial role of mitochondrial fission dependent on Drp1 in the diabetic myocardium subjected to I/R, and strongly indicates that Drp1 inhibition may restore the cardioprotective effect of SevP in diabetic rats.

Project description:BackgroundThe diabetic heart exhibits a high sensitivity to ischaemia/reperfusion (I/R) injury. Diabetes mellitus (DM) can affect the efficacy of cardioprotective interventions and reduce the therapeutic potential of existing treatment options. This study aimed to investigate the feasibility of shifting from monotherapy to combination therapy in diabetic myocardial I/R injury.Methods6-8 week rats were randomized into 10 groups: sham, I/R, ischaemia postconditioning (I-Post), nicorandil (Nic), combination therapy (I-Post + Nic), DM sham, DM I/R, DM I-Post, DM Nic and DM I-Post + Nic. The extent of myocardial injury was clarified by measuring CK-MB and NO levels in plasma, ROS content in myocardial tissues, and TTC/Evans Blue staining to assess the area of myocardial infarction. Pathological staining of cardiac tissue sections were performed to clarify the structural changes in myocardial histopathology. Finally, Western blotting was performed to detect the phosphorylation levels of some key proteins in the PI3K/Akt signalling pathway in myocardial tissues.ResultsWe confirms that myocardial injury in diabetic I/R rats remained at a high level after treatment with I-Post or nicorandil alone. I-Post combined with nicorandil showed better therapeutic effects in diabetic I/R rats, and the combined treatment further reduced the area of myocardial injury in diabetic I/R rats compared with I-Post or nicorandil treatment alone (P < 0.001), as well as the levels of the myocardial injury markers CK-MB and ROS (P < 0.001); it also significantly increased plasma NO levels. Pathological staining also showed that diabetic rats benefited significantly from the combination therapy. Further mechanistic studies confirmed this finding. The protein phosphorylation levels of PI3K/Akt signalling pathway in the heart tissue of diabetic I/R rats were significantly higher after the combination treatment than after one treatment alone (all P < 0.05).ConclusionI-Post combined with nicorandil treatment maintains effective cardioprotection against diabetic myocardial I/R injury by activating the PI3K/Akt signalling pathway.

Project description:During acute reperfusion, the expression profiles of long noncoding RNAs in adult rats with focal cerebral ischemia undergo broad changes. However, whether long noncoding RNAs are involved in neuroprotective effects following focal ischemic stroke in rats remains unclear. In this study, RNA isolation and library preparation was performed for long noncoding RNA sequencing, followed by determining the coding potential of identified long noncoding RNAs and target gene prediction. Differential expression analysis, long noncoding RNA functional enrichment analysis, and co-expression network analysis were performed comparing ischemic rats with and without ischemic postconditioning rats. Rats were subjected to ischemic postconditioning via the brief and repeated occlusion of the middle cerebral artery or femoral artery. Quantitative real-time reverse transcription-polymerase chain reaction was used to detect the expression levels of differentially expressed long noncoding RNAs after ischemic postconditioning in a rat model of ischemic stroke. The results showed that ischemic postconditioning greatly affected the expression profile of long noncoding RNAs and mRNAs in the brains of rats that underwent ischemic stroke. The predicted target genes of some of the identified long noncoding RNAs (cis targets) were related to the cellular response to ischemia and stress, cytokine signal transduction, inflammation, and apoptosis signal transduction pathways. In addition, 15 significantly differentially expressed long noncoding RNAs were identified in the brains of rats subjected to ischemic postconditioning. Nine candidate long noncoding RNAs that may be related to ischemic postconditioning were identified by a long noncoding RNA expression profile and long noncoding RNA-mRNA co-expression network analysis. Expression levels were verified by quantitative real-time reverse transcription-polymerase chain reaction. These results suggested that the identified long noncoding RNAs may be involved in the neuroprotective effects associated with ischemic postconditioning following ischemic stroke. The experimental animal procedures were approved by the Animal Experiment Ethics Committee of Kunming Medical University (approval No. KMMU2018018) in January 2018.

Dataset Information

Protective effects of postconditioning in transvaginally created pneumoperitoneum.

Publications

Protective effects of postconditioning in transvaginally created pneumoperitoneum.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets