morroniside and Inflammation

Inflammation is closely associated with the pathogenesis of various ocular diseases. Uveitis is a condition characterized by the inflammation of the uvea and ocular tissues that causes extreme pain, decreases visual acuity, and may eventually lead to blindness. The pharmacological functions of morroniside, isolated from. An endotoxin-induced uveitis (EIU) mouse model was constructed and treated with morroniside. The inflammatory response was observed using slit lamp microscopy, and histopathological changes were observed by hematoxylin-eosin staining. The cell count in the aqueous humor was measured using a hemocytometer. The concentrations of TNF-. Morroniside effectively ameliorated the inflammatory response in EIU mice. Furthermore, morroniside significantly reduced the concentrations of IL-1. Collectively, these findings suggest that morroniside may protect against LPS-induced inflammation in uveitis by promoting M2 polarization through the inhibition of the JAK/STAT pathway.

Topics: Animals; Anti-Inflammatory Agents; Ciliary Body; Endotoxins; Inflammation; Interleukin-6; Janus Kinases; Lipopolysaccharides; Macrophages; Mice; Signal Transduction; STAT Transcription Factors; Tumor Necrosis Factor-alpha; Uveitis

To investigate the effects of morroniside on inflammatory and oxidative stress in lipopolysaccharide (LPS)-induced inflammatory bowel disease (IBD) cell model.. NCM460 cells were treated with 2-, 5-, or 10-μg/mL LPS for 24 h to develop an IBD cell model. MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) colorimetric assay was performed to uncover the role of morroniside on the viability of LPS-treated NCM460 cells. Flow cytometry and immunoblot assays were performed to confirm the effects of morroniside on the apoptosis of LPS-treated NCM460 cells. Quantitative polymerase chain reaction and enzyme-linked-immunosorbent serologic assays were performed to confirm the effects of morroniside on inflammatory and oxidative stress by measuring the levels of tumor necrosis factor-α, interleukin-1β, IL-6, superoxide dismutase, malondialdehyde, total antioxidant capacity, and myeloperoxidase. In addition, immunoblot and immunofluorescence assays were performed to detect the effects of morroniside on NLRP3 and NF-κB pathways.. Monosine attenuated LPS-induced injury of NCM460 cells. Monosine reduced LPS-induced inflammation in NCM460 cells. In addition, morroniside reduced LPS-induced oxidative stress in NCM460 cells. Mechanically, morroniside suppressed NLRP3 and NF-κB pathways, and alleviated LPS-induced inflammatory and oxidative stress in IBD.. Morroniside could serve as a promising drug for treating IBD.

Topics: Humans; Inflammation; Inflammatory Bowel Diseases; Lipopolysaccharides; NF-kappa B; NLR Family, Pyrin Domain-Containing 3 Protein; Oxidative Stress; Signal Transduction

Osteoarthritis (OA) is a common degenerative disease that results in joint inflammation as well as pain and stiffness. A previous study has reported that

Topics: Animals; Cartilage, Articular; Chondrocytes; Cornus; Cyclooxygenase 2; Dinoprostone; Disease Models, Animal; Gene Expression Regulation; Glycosides; Humans; Inflammation; Interleukin-1beta; Matrix Metalloproteinase 13; Matrix Metalloproteinase 3; Menisci, Tibial; Mice; Osteoarthritis; Plant Extracts; Primary Cell Culture; RAW 264.7 Cells; Signal Transduction

Treating the vascular elements within the neurovascular unit is essential for protecting and repairing the brain after stroke. Acute injury on endothelial systems results in the disruption of blood-brain barrier (BBB), while post-ischemic angiogenesis plays an important role in delayed functional recovery. Here, we considered alterations in microvessel integrity to be targets for brain recovery, and tested the natural compound morroniside as a therapeutic approach to restore the vascular elements of injured tissue in a rat model of focal cerebral ischemia. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) model, and morroniside was then administered intragastrically once a day at doses of 30, 90, and 270 mg/kg. BBB integrity and associated factors were analyzed to identify cerebrovascular permeability 3 days after MCAO. The recruitment of endothelial progenitor cells (EPCs), the expression of angiogenic factors and the new vessel formation in the peri-infarct cortex of rats were examined 7 days after MCAO to identify the angiogenesis. We demonstrated that at 3 days post-ischemia, morroniside preserved neurovascular unit function by ameliorating BBB injury. By 7 days post-ischemia, morroniside amplified angiogenesis, in part by enhancing endothelial progenitor cell proliferation and expression of angiogenic factors. Morever, the increase in the amount of vWF+ vessels induced by ischemia could be extended to 28 days after administration of morroniside, indicating the crucial role of morroniside in angiogenesis during the chronic phase. Taken together, our findings suggested that morroniside might offer a novel therapeutic approach for promoting microvascular integrity recovery and provide a thoroughly new direction for stroke therapy.

Topics: Animals; Blood-Brain Barrier; Brain Ischemia; Capillary Permeability; Cell Proliferation; Cerebral Cortex; Endothelial Cells; Glycosides; Infarction, Middle Cerebral Artery; Inflammation; Male; Matrix Metalloproteinases; Microvessels; Models, Biological; Neovascularization, Physiologic; Rats, Sprague-Dawley; Receptor, TIE-2; von Willebrand Factor

The present study was conducted to examine whether morroniside has an ameliorative effect on diabetes-induced alterations such as oxidative stress, inflammation, and apoptosis in the liver of type 2 diabetic db/db mice. Morroniside (20 or 100 mg/kg body weight/d, per os (p.o.)) was administered every day for 8 weeks to db/db mice, and its effect was compared with vehicle-treated db/db and m/m mice. The administration of morroniside decreased the elevated serum glucose concentration in db/db mice, and reduced the increased oxidative biomarkers including the generation of reactive oxygen species and lipid peroxidation in the liver. The db/db mice exhibited the up-regulation of nicotinamide adenine dinucleotide phosphate oxidase subunits, NF-E2-related factor 2 (Nrf2), heme oxygenase-1, nuclear factor-kappa B, cyclooxygenase-2, inducible nitric oxide synthase, monocyte chemotactic protein-1, and intracellular adhesion molecule-1 levels in the liver; however, morroniside treatment significantly reduced those expressions. Moreover, the augmented expressions of apoptosis-related proteins, Bax and cytochrome c, were down-regulated by morroniside administration. Hematoxylin-eosin staining showed that the increased hepatocellular damage in the liver of db/db mice improved on morroniside administration. Taking these into consideration, our findings support the therapeutic evidence for morroniside ameliorating the development of diabetic hepatic complications via regulating oxidative stress, inflammation, and apoptosis.

Topics: Animals; Antioxidants; Apoptosis; Blood Glucose; Cornus; Cyclooxygenase 2; Diabetes Mellitus, Type 2; Drug Evaluation, Preclinical; Glycosides; Heme Oxygenase-1; Histones; Hypoglycemic Agents; Inflammation; Iridoid Glycosides; Liver; Liver Function Tests; Male; Mice; Mice, Inbred C57BL; Molecular Targeted Therapy; NF-E2-Related Factor 2; Oxidative Stress; Phytotherapy; Plant Preparations; Reactive Oxygen Species; Thiobarbituric Acid Reactive Substances; Transcription Factor RelA

The effects of morroniside isolated from Corni Fructus on renal lipids and inflammation provoked by hyperglycaemia were investigated using type 2 diabetic mice.. Morroniside was administered orally to db/db mice at 20 or 100 mg/kg daily for 8 weeks, and its effects were compared with those in vehicle-treated db/db and m/m (non-diabetic) mice. Serum and renal biochemical factors and protein expression related to lipid homeostasis and inflammation were measured.. Morroniside produced significant dose-dependent reductions in serum triglyceride and renal glucose and lipid levels. Morroniside altered the abnormal protein expression of sterol regulatory element binding proteins (SREBP-1 and SREBP-2). In addition, the formation of reactive oxygen species and lipid peroxidation were inhibited in the morroniside-treated db/db mouse group, and the ratio of reduced glutathione to the oxidised form was significantly elevated. These results suggest that morroniside alleviated oxidative stress in the kidneys of db/db mice. Furthermore, 100 mg/kg morroniside down-regulated the expression of nuclear factor-kappaBp65, cyclooxygenase-2 and inducible nitric oxide synthase augmented in db/db mice.. Morroniside may inhibit abnormal lipid metabolism and inflammation due to reactive oxygen species in the kidneys in type 2 diabetes.

Topics: Animals; Biomarkers; Cornus; Cyclooxygenase 2; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Dose-Response Relationship, Drug; Fruit; Glucose; Glycosides; Inflammation; Lipid Metabolism; Male; Mice; Mice, Inbred C57BL; Nitric Oxide Synthase Type I; Oxidative Stress; Plants, Medicinal; Sterol Regulatory Element Binding Proteins; Transcription Factor RelA; Triglycerides