lignans has been researched along with Postoperative-Complications* in 5 studies
5 other study(ies) available for lignans and Postoperative-Complications
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SIRT3 activator honokiol ameliorates surgery/anesthesia-induced cognitive decline in mice through anti-oxidative stress and anti-inflammatory in hippocampus.
Increasing evidence indicates that neuroinflammatory and oxidative stress play two pivotal roles in cognitive impairment after surgery. Honokiol (HNK), as an activator of Sirtuin3 (SIRT3), has potential multiple biological functions. The aim of these experiments is to evaluate the effects of HNK on surgery/anesthesia-induced cognitive decline in mice.. Adult C57BL/6 mice received a laparotomy under sevoflurane anesthesia and HNK or SIRT3 inhibitor (3-TYP) treatment. Cognitive function and locomotor activity of mice were evaluated using fear conditioning test and open field test on postoperative 1 and 3 days. Neuronal apoptosis in CA1 and CA3 area of hippocampus was examined using TUNEL assay. And Western blot was applied to measure the expression of pro-inflammatory cytokines and SIRT3/SOD2 signaling-associated proteins in hippocampus. Meanwhile, SIRT3 positive cells were calculated by immunohistochemistry. The mitochondrial membrane potential, malondialdehyde (MDA), and mitochondrial radical oxygen species (mtROS) were detected using standard methods.. Honokiol attenuated surgery-induced memory loss and neuronal apoptosis, decreased neuroinflammatory response, and ameliorated oxidative damage in hippocampus. Notably, surgery/anesthesia induced an obviously decrease in hippocampal SIRT3 expression, whereas the HNK increased SIRT3 expression and thus decreased the acetylation of superoxide dismutase 2 (SOD2). However, 3-TYP treatment inhibited the HNK's rescuing effects.. These results suggested that activation of SIRT3 by honokiol may attenuate surgery/anesthesia-induced cognitive impairment in mice through regulation of oxidative stress and neuroinflammatory in hippocampus. Topics: Anesthesia; Anesthetics, Inhalation; Animals; Anti-Inflammatory Agents; Biphenyl Compounds; Cognitive Dysfunction; Female; Hippocampus; Inflammation; Laparotomy; Lignans; Mice, Inbred C57BL; Nootropic Agents; Oxidative Stress; Postoperative Complications; Random Allocation; Sevoflurane; Sirtuin 3 | 2019 |
Honokiol-Mediated Mitophagy Ameliorates Postoperative Cognitive Impairment Induced by Surgery/Sevoflurane via Inhibiting the Activation of NLRP3 Inflammasome in the Hippocampus.
The potential mechanism of postoperative cognitive impairment is still largely unclear. The activation of NLRP3 inflammasome had been reported to be involved in neurodegenerative diseases, including postoperative cognitive change, and is closely related to mitochondrial ROS and mitophagy. Honokiol (HNK) owns multiple organic protective effects. This study is aimed at observing the neuroprotective effect of HNK in postoperative cognitive change and examining the role of HNK in the regulation of mitophagy and the relationship between these effects and NLRP3 inflammasome activation in mice induced by surgery/anesthesia.. In this study, mice were divided into several groups: control group, surgery group, surgery+HNK group, and surgery+HNK+3-methyladenine (3-MA) group. Hippocampal tissue samples were harvested and used for proinflammatory cytokines, mitochondrial ROS, and malondialdehyde (MDA) assay. The process of mitophagy and the activation of NLRP3 inflammasome were observed by Western blot, immunohistochemistry, and transmission electron microscopy.. The results showed that HNK treatment obviously recovered the postoperative decline and enhanced the expressions of LC3-II, Beclin-1, Parkin, and PINK1 at protein levels after surgery/sevoflurane treatment, which are both an autophagy marker and a mitophagy marker. In addition, HNK attenuated mitochondrial structure damage and reduced mtROS and MDA generation, which are closely associated with NLRP3 inflammasome activation. Honokiol-mediated mitophagy inhibited the activation of NLRP3 inflammasome and neuroinflammation in the hippocampus. Using 3-MA, an autophagy inhibitor, the neuroprotective effects of HNK on mitophagy and NLRP3 inflammasome activation were eliminated.. These results indicated that HNK-mediated mitophagy ameliorates postoperative cognitive impairment induced by surgery/sevoflurane. This neuroprotective effect may be involved in inhibiting the activation of NLRP3 inflammasome and suppressing inflammatory responses in the hippocampus. Topics: Animals; Apoptosis; Autophagy; Biphenyl Compounds; Cognitive Dysfunction; Dentate Gyrus; Female; Hippocampus; Inflammasomes; Lignans; Mice, Inbred C57BL; Microglia; Mitochondria; Mitophagy; Neurons; NLR Family, Pyrin Domain-Containing 3 Protein; Oxidative Stress; Postoperative Complications; Reactive Oxygen Species; Sevoflurane | 2019 |
Therapeutic Action of Honokiol on Postoperative Ileus via Downregulation of iNOS Gene Expression.
Postoperative ileus is a common complication after intra-abdominal surgery. Nitric oxide produced by macrophages in the inflamed gastrointestinal tract plays a crucial role in the pathogeny of postoperative ileus. Honokiol, extracted from the bark of Magnolia spp., is a natural compound with a biphenolic structure. In the present study, we examined the effect of honokiol on postoperative ileus and discussed its site of action. Postoperative ileus model mice were generated by surgical intestinal manipulation. Mice were administered honokiol (10 mg kg Topics: Animals; Biphenyl Compounds; Cytokines; Down-Regulation; Gastrointestinal Motility; Ileus; Inflammation Mediators; Leukocytes; Lignans; Macrophages, Peritoneal; Mice; Nitric Oxide Synthase Type II; Postoperative Complications; RNA, Messenger | 2017 |
Honokiol decreases intra-abdominal adhesion formation in a rat model.
The purpose of this study was to investigate the effectiveness of honokiol, a natural molecule that was shown to have antioxidant effects, in prevention of intra-abdominal adhesion formation in a rat model.. This study was conducted on a total of 40 non-pregnant Sprague-Dawley rats, which were divided into 4 groups as follows: sham, control, saline, and honokiol groups. Both uterine horns of the rats in control, saline, and honokiol groups were exposed and a 2-cm segment of the anti-mesenteric surface of both uterine horns was traumatized by a scalpel. The saline group was administered 2 ml of saline/day intraperitoneally for 5 days after the operation. The honokiol group, on the other hand, was administered honokiol intraperitoneally at a dose of 1 mg/kg/day for 5 days after the operation. On postoperative day 14, 3 ml of intracardiac blood sample was taken from the rats for biochemical analyses, and the rats were sacrificed this way.. Adhesion and inflammation scores were significantly lower in the honokiol group compared with the saline and control groups (p < 0.008). Similarly, fibrosis score was significantly lower in the honokiol group compared with the saline group (p < 0.008).. Honokiol was found to be effective in prevention of intra-abdominal adhesion formation in a rat model. However, larger studies are needed to shed light on the exact role of honokiol in intra-abdominal adhesion formation and to determine the molecular aspects of the promising results found in this study. Topics: Animals; Antioxidants; Biphenyl Compounds; Disease Models, Animal; Female; Lignans; Postoperative Complications; Rats; Rats, Sprague-Dawley; Tissue Adhesions; Uterus | 2015 |
Taiwanin A incorporated polyurethane fiber sheets for prevention of postoperative cancer recurrence.
In this study, we propose a single solution for prevention of postoperative complications and recurrence of highly metastatic gastrointestinal tract cancers. Here, we demonstrate preparation and characterization of Taiwanin A incorporated polyurethane fiber sheets with excellent mechanical properties and sustained drug release. Sheets with elastic modulus of 8 MPa and ultimate tensile strength of 30 MPa will provide support on surgical staple line preventing leakage at anastomosis. Slight burst release of the drug within 7 days (15%) and further sustained release will inhibit proliferation and migration of remaining cancer cells and maintain locoregional high drug concentration to prevent recurrence of the disease. High elasticity of the material will promote healing process without impeding natural peristalsis movement of gastrointestinal organs. Topics: 3T3 Cells; Anastomotic Leak; Animals; Antineoplastic Agents, Phytogenic; Biocompatible Materials; Cell Line, Tumor; Cell Movement; Cell Survival; Combined Modality Therapy; Delayed-Action Preparations; Drug Delivery Systems; Drug Liberation; Elastic Modulus; Furans; Gastrointestinal Neoplasms; Humans; Lignans; Membranes, Artificial; Mice; Neoplasm Recurrence, Local; Polyurethanes; Postoperative Complications; Surface Properties; Tensile Strength | 2015 |