acteoside and Reperfusion-Injury

Topics: Animals; Endothelial Cells; Hepatocytes; HMGB1 Protein; Hypoxia; Liver; Mice; Reperfusion Injury; Toll-Like Receptor 3

This study aims to show the corrective effect of verbascoside on histomorphological and biochemical differences in the colon mucosa of rats in which colon ischemia-reperfusion (I/R) injury was induced.. Fifty Sprague Dawley male rats were divided into 5 groups, of control, sham, ischemia (I), I/R, and I/R+verbascoside. Ischemia and reperfusion were applied to the suitable groups for 30 minutes and 120 minutes respectively, and 10 mg/kg verbascoside was administered intraperitoneally. Histomorphological assessment was done in the colon tissues obtained, and the goblet cells were assessed using the Alcian blue method. Proliferating cell nuclear antigen (PCNA), TUNEL, and hypoxia-induced factor 1 (HIF-1α) assays were used to assess oxidative stress with the immunohistochemical method. Malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), and total thiol (TT) levels were checked, for a biochemical analysis of oxidative stress.. Compared with the I/R group, histomorphological differences were seen to be corrected in colon epithelium in the I/ R+verbascoside group. The goblet cell number increased and cell proliferation was increased, as seen with the PCNA assay; and apoptosis was decreased, as seen with the TUNEL assay. HIF-1α expression also decreased in the drug group. In the drug group, SOD, GSH-Px, TAS, and TT levels increased, but TOS, OSI, and MDA levels decreased.. It was seen that verbascoside had a corrective effect on histomorphological and biochemical differences caused by I/R injury.

Topics: Animals; Antioxidants; Colon; Disease Models, Animal; Glucosides; Intestinal Mucosa; Male; Oxidative Stress; Phenols; Rats; Rats, Sprague-Dawley; Reperfusion Injury

The objective of this study is to investigate the roles of acteoside (ACT) in cells with oxygen-glucose deprivation and reoxygenation (OGD/R)-induced injury and the underlying mechanisms. The differentially expressed genes (DEGs) in rats with middle cerebral artery occlusion were identified using GSE61616 data set. Kyoto Encyclopedia of Genes and Genomes pathway enrichment with the DEGs and the prediction of ACT's targets were conducted using The Comparative Toxicogenomics Database. The OGD/R model was established with bEnd.3 cells. Following that, bEnd.3 cells were treated by distinct concentrations of ACT and IL-10. The proliferation and apoptosis of cells were analyzed by cell counting kit-8 and flow cytometry assays, respectively. Western blot was used to check involved proteins. Herein, we identified CCL2, CXCL10, and ICAM1 as the targets of ACT, which were upregulated in tissues of MACO rats and cells with OGD/R-induced injury. ACT promoted the proliferation but reduce the apoptosis of cells with OGD/R-induced injury. Moreover, these effects of ACT were enhanced by IL-10. After being treated with ACT, IL-10, or ACT together with IL-10, the levels of CCL2, CXCL10, and ICAM1 were all decreased, whereas p-Stat3 was raised in cells with OGD/R-induced injury, while Stat3 expression presented no significant difference among groups. ACT protected cells against OGD/R-induced injury through regulating the IL-10/Stat3 signaling, indicating that ACT might be an effective therapy drug to lower cerebral ischemia/reperfusion injury.

Topics: Animals; Apoptosis; Cell Hypoxia; Cell Line; Cell Proliferation; Chemokine CCL2; Chemokine CXCL10; Glucosides; Intercellular Adhesion Molecule-1; Interleukin-10; Oxygen; Phenols; Protective Agents; Rats; Reperfusion Injury; Signal Transduction; STAT3 Transcription Factor; Up-Regulation

The objective of this study was to assess the anti-stroke activity of acteoside isolated from methanolic root extract of C. oppositifolia METHODS: Ischemia-reperfusion(I/R) brain injury was induced in Wistar rats to assess the anti-stroke activity of acteoside. Rats were pretreated with acteoside (10, 25 & 50 mg/kg, p.o.) before the induction of I/R injury. Parameters such as neurological, motor-cognitive functions were evaluated along with morphological (brain volume, infarct size), biochemical (SOD, Catalase, GSH, lipid peroxidation, TNF-α, IL-6, IL-10, ICAM-1, HIF-1α, VEGF, and NF-κB), histopathological, and gene expression studies (HIF-1α, VEGF) were performed to study the protective effect of acteoside against I/R induced brain injury.. I/R injury caused significant deterioration of neurological (p < 0.01), motor (p < 0.01) and cognitive (p < 0.01) functions, associated with increase in the brain volume (p < 0.01), and infarct size (p < 0.01); increase in the levels of MDA, TNF-α, IL-6, ICAM-1, HIF-1α, VEGF, and NF-κB along with significant decrease in SOD, catalase, GSH, and IL-10 (p < 0.01 for all parameters) compared to Sham control group. Histology of brain tissue of disease control group exhibited significant vascular changes, neutrophil infiltration, cerebral oedema, and necrosis of the neuronal cells. Further, the gene-expression studies showed significant increase in the HIF-1α (p < 0.01) and VEGF (p < 0.01) mRNA levels in the I/R control compared to Sham control. Interestingly, the acteoside (10, 25 & 50 mg/kg) has prevented the neurological, motor and cognitive dysfunctions, along with inhibiting the morphological, biochemical, histological and gene expression changes induced by I/R-injury (p < 0.05 for 10 mg; p < 0.01 for 25 & 50 mg/kg of acteoside for all the parameters).. These findings suggest that acteoside possess potent anti-stroke activity through modulation of HIF-1α, NF-κB, and VEGF pathway along with its potent antioxidant activity.

Topics: Animals; Antioxidants; Disease Models, Animal; Dose-Response Relationship, Drug; Glucosides; Hypoxia-Inducible Factor 1, alpha Subunit; Lamiaceae; Male; NF-kappa B; Phenols; Plant Extracts; Rats; Rats, Wistar; Reperfusion Injury; Stroke; Vascular Endothelial Growth Factor A

Acteoside (ACT) has been shown to exert antioxidant and neuroprotective effects in neurodegenerative diseases. However, the effect of ACT on cerebral ischemia-reperfusion (I/R) injury is not yet clear. In this study, we found that ACT administration reduced infarct volume and brain edema, and improved neurological deficits, as indicated by the decreased modified neurological severity score. Administration of ACT strikingly reduced oxidative stress, accompanied by decreased levels of reactive oxygen species and malondialdehyde and increased levels of superoxide dismutase and catalase in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). Furthermore, ACT administration reduced the number of terminal deoxynucleotidyl transferase uridine 5'-triphosphate (UTP) nick-end labeling-positive cells in the cerebral cortex of ischemic side of MCAO/R rats, accompanied by downregulation of B cell lymphoma 2 (Bcl-2) associated X protein and cleaved caspase-3 proteins and upregulation of Bcl-2 protein. Additionally, ACT treatment inhibited the protein kinase R/eukaryotic initiation factor-2α stress pathway in the brains of MCAO/R rats. Our results demonstrated that ACT attenuates oxidative stress and neuronal apoptosis in MCAO/R rats, suggesting that ACT may serve as a novel therapeutic candidate for the treatment of I/R brain injury.

Topics: Animals; Antioxidants; Apoptosis; bcl-2-Associated X Protein; Brain; Brain Injuries; Brain Ischemia; Caspase 3; Glucosides; Infarction, Middle Cerebral Artery; Ischemia; Magnoliopsida; Male; Neuroprotective Agents; Oxidative Stress; Phenols; Phytotherapy; Plant Extracts; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; Rats, Wistar; Reperfusion Injury; Superoxide Dismutase; Up-Regulation

Topics: Animals; Bepridil; Biphenyl Compounds; Caffeic Acids; Coumaric Acids; Free Radicals; Glucosides; In Vitro Techniques; Lipid Peroxidation; Liver; Male; Mitochondria, Liver; Oxygen Consumption; Phenols; Picrates; Plant Extracts; Rats; Rats, Wistar; Reperfusion Injury; Vitamin E