monascin and Disease-Models--Animal

Increasing evidence verified that oxidative stress and neuroinflammatory response exacerbates motor deficits and increases neuronal loss in several rodent models of Parkinson's disease. In the present study, we explore the neuroprotective effects of monascin in a rotenone-induced Parkinson's disease model as well as the underlying mechanisms. Our results showed that monascin remarkedly attenuated behavioral impairments and the depletion of dopaminergic neurons induced by rotenone in the rats. Besides, monascin decreased the levels of pro-inflammatory factors such as interleukin-1β, interleukin-6, tumor necrosis factor-α and oxidative stress marker malondialdehyde while promoted the expression of superoxide dismutase, glutathione peroxidase and other antioxidant factors. Further detection of the expression of related proteins showed that monascin significantly promoted the expression of proliferator-activated receptor-gamma, F-E2-related factor 2 and heme oxygenase-1, but inhibited the expression of NF-κB. What's more, levels of growth factors that are essential for neuronal and synaptic function were increased under the effects of monascin. All in all, our results revealed that monascin exerted neuroprotective effects in rotenone model of Parkinson's disease via antioxidation and anti-neuroinflammation.

Topics: Animals; Disease Models, Animal; Dopaminergic Neurons; Encephalitis; Heterocyclic Compounds, 3-Ring; Male; Neuroprotective Agents; Oxidative Stress; Parkinson Disease; Parkinsonian Disorders; Rats, Sprague-Dawley; Rotenone

Osteoarthritis (OA) is an age-related degenerative disease and is the fourth major cause of disability, but there are no effective therapies because of its complex pathology and the side effects of the drugs. Previous research demonstrated that inflammation and ECM degradation play major roles in OA development. Monascin is an azaphilonoid pigment extracted from Monascus-fermented rice with a potential anti-inflammatory effect reported in various preclinical studies. In the present study, we investigated the protectiveness of monascin on interleukin (IL)-1β-induced mouse chondrocytes and surgical destabilization of the medial meniscus mouse (DMM) OA models. In vitro, monascin treatment inhibited the IL-1β-induced expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), nitric oxide (NO), prostaglandin E

Topics: Animals; Chondrocytes; Cyclooxygenase 2; Dinoprostone; Disease Models, Animal; Female; Heterocyclic Compounds, 3-Ring; Humans; Interleukin-1beta; Male; Mice; Mice, Inbred C57BL; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Osteoarthritis; Signal Transduction

Intracerebral hemorrhage (ICH) is a particularly devastating form of stroke with high mortality and morbidity. Hematomas are the primary cause of neurologic deficits associated with ICH. The products of hematoma are recognized as neurotoxins and the main contributors to edema formation and tissue damage after ICH. Finding a means to efficiently promote absorption of hematoma is a novel clinical challenge for ICH. Peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor erythroid 2-related factor 2 (Nrf2), had been shown that, can take potential roles in the endogenous hematoma clearance. However, monascin, a novel natural Nrf2 activator with PPARγ agonist, has not been reported to play a role in ICH. This study was designed to evaluate the effect of monascin on neurological deficits, hematoma clearance and edema extinction in a model of ICH in rats.. 164 adult male Sprague-Dawley (SD) rats were randomly divided into sham; vehicle; monascin groups with low dosages (1mg/kg/day), middle dosages (5mg/kg/day) and high dosages (10mg/kg/day) respectively. Animals were euthanized at 1, 3 and 7days following neurological evaluation after surgery. We examined the effect of monascin on the brain water contents, blood brain barrier (BBB) permeability and hemoglobin levels, meanwhile reassessed the volume of hematoma and edema around the hematoma by Magnetic Resonance Imaging (MRI) in each group.. The high dosage of monascin significantly improved neurological deficits, reduced the volume of hematoma in 1-7days after ICH, decreased BBB permeability and edema formation in 1-3days following ICH.. Our study demonstrated that the high dosage of monascin played a neuroprotective role in ICH through reducing BBB permeability, edema and hematoma volume.

Topics: Animals; Blood-Brain Barrier; Brain Edema; Capillary Permeability; Cerebral Hemorrhage; Disease Models, Animal; Dose-Response Relationship, Drug; Hematoma; Heterocyclic Compounds, 3-Ring; Male; Neuroprotective Agents; NF-E2-Related Factor 2; PPAR gamma; Random Allocation; Rats, Sprague-Dawley

This experiment established the ovariectomized (OVX) rat model of postmenopausal osteoporosis and examined the effect of the oral administration of different dosages of dioscorea, red mold dioscorea (RMD), and soy isoflavones on bone mineral density (BMD). Three months after osteoporosis had been induced and 4 weeks after feeding had begun, the tibia and femur BMD of OVX rats administered RMD showed significant increases compared with that of all other groups of OVX rats. Closer examination using microcomputed tomography also revealed that the RMD-administered rats had denser trabecular bone volume and a higher trabecular number compared to all other rat groups. Reconstructed 3D imaging indicated increases in cancellous bone mineral content, cancellous bone mineral density, and cortical bone mineral content of the proximal tibia in OVX rats. These findings indicate that administration of monacolin K and phytoestrogen diosgenin could prevent bone loss induced by estrogen deficiency.

Topics: Animals; Bone Density; Dioscorea; Diosgenin; Disease Models, Animal; Female; Fermentation; Flavins; Glycine max; Heterocyclic Compounds, 3-Ring; Isoflavones; Lovastatin; Monascus; Osteoporosis; Ovariectomy; Phytoestrogens; Plant Roots; Rats; Rats, Sprague-Dawley