myricitrin has been researched along with Osteoporosis* in 2 studies
1 review(s) available for myricitrin and Osteoporosis
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Effects of Myricitrin and Relevant Molecular Mechanisms.
In humans, oxidative stress is thought to be involved in the development of Parkinson's disease, Alzheimer's disease, atherosclerosis, heart failure, myocardial infarction and depression. Myricitrin, a botanical flavone, is abundantly distributed in the root bark of Myrica cerifera, Myrica esculenta, Ampelopsis grossedentata, Nymphaea lotus, Chrysobalanus icaco, and other plants. Considering the abundance of its natural sources, myricitrin is relatively easy to extract and purify. Myricitrin reportedly possesses effective anti-oxidative, anti-inflammatory, and anti-nociceptive activities, and can protect a variety of cells from in vitro and in vivo injuries. Therefore, our current review summarizes the research progress of myricitrin in cardiovascular diseases, nerve injury and anti-inflammatory, and provides new ideas for the development of myricitrin. Topics: Alzheimer Disease; Animals; Anti-Inflammatory Agents; Cardiovascular Diseases; Flavonoids; Humans; Inflammation; Myrica; Osteoporosis; Oxidative Stress; Parkinson Disease; Phytotherapy | 2020 |
1 other study(ies) available for myricitrin and Osteoporosis
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Protective effects of myricitrin against osteoporosis via reducing reactive oxygen species and bone-resorbing cytokines.
Oxidative stress is a crucial pathogenic factor in the development of osteoporosis. Myricitrin, isolated from Myrica cerifera, is a potent antioxidant. We hypothesized that myricitrin possessed protective effects against osteoporosis by partially reducing reactive oxygen species (ROS) and bone-resorbing cytokines in osteoblastic MC3T3-E1 cells and human bone marrow stromal cells (hBMSCs). We investigated myricitrin on osteogenic differentiation under oxidative stress. Hydrogen peroxide (H2O2) was used to establish an oxidative cell injury model. Our results revealed that myricitrin significantly improved some osteogenic markers in these cells. Myricitrin decreased lipid production and reduced peroxisome proliferator-activated receptor gamma-2 (PPARĪ³2) expression in hBMSCs. Moreover, myricitrin reduced the expression of receptor activator of nuclear factor kappa-B ligand (RANKL) and IL-6 and partially suppressed ROS production. In vivo, we established a murine ovariectomized (OVX) osteoporosis model. Our results demonstrated that myricitrin supplementation reduced serum malondialdehyde (MDA) activity and increased reduced glutathione (GSH) activity. Importantly, it ameliorated the micro-architecture of trabecular bones in the 4th lumbar vertebrae (L4) and distal femur. Taken together, these results indicated that the protective effects of myricitrin against osteoporosis are linked to a reduction in ROS and bone-resorbing cytokines, suggesting that myricitrin may be useful in bone metabolism diseases, particularly osteoporosis. Topics: Adult; Aged; Animals; Bone and Bones; Bone Density; Cell Differentiation; Cell Line; Female; Flavonoids; Histocytochemistry; Humans; Interleukin-6; Male; Mice; Mice, Inbred BALB C; Middle Aged; Osteoporosis; Oxidative Stress; PPAR gamma; Random Allocation; RANK Ligand; Reactive Oxygen Species | 2014 |