Supplementation of nanofiltrated deep ocean water ameliorate the progression of osteoporosis in ovariectomized rat via regulating osteoblast differentiation.

Magnesium was reported to be necessary for bone formation. Previous study indicated nanofiltrated deep ocean water (DOW) rich in magnesium. This study investigated the potential mechanisms of DOW in ameliorating osteoporosis. Briefly, female Sprague-Dawley rat was ovariectomized and fed with 0.35, 0.7, or 1.4 ml/kg of DOW daily for 8 weeks. In the results, DOW increased bone density, decreased trabecular bone loss, and decreased bone adiposity. DOW improved bone mass by examining structure in micro-computed tomography. About 0.35 and 0.7 ml/kg of DOW can increase protein expression of runt-related transcription factor 2 (RUNX2), an essential transcription factor for regulating osteoblast differentiation, by 9.4% or 12.9%. In human osteoblast, DOW increased the levels of osteocalcin, RUNX2, and alkaline phosphatase; all the proteins can regulate osteoblast differentiation. Considering the results of in vivo and in vitro study, DOW can ameliorate ovareictomy-caused osteoporosis via regulating the osteoblast differentiation, thereby, maintenance of bone structure. PRACTICAL APPLICATIONS: In addition to calcium, magnesium is essential to promoting the deposition of calcium in bones and regulating its transport; it may also slow the progression of osteoporosis. Nanofiltrated DOW contains abundant magnesium along with several microelements and peptides. In this study, a product was developed for decelerating osteoporosis by using an estrogen depletion model. DOW regulates osteoblast differentiation and thus prevents osteoporosis. This finding provides an alternative healthy source of bone supplements. In addition to tablets or capsules, aqueous supplements can be produced to achieve osteoporosis prevention. This finding is beneficial to the health-care industry for developing sustainable supplements.

Solanum nigrum Polyphenol Extracts Inhibit Hepatic Inflammation, Oxidative Stress, and Lipogenesis in High-Fat-Diet-Treated Mice.

Patients with diabetes, obesity, and hyperlipidemia are all high-risk groups for fatty liver; however, the mechanism of fatty liver formation is not completely understood. Studies have indicated that abnormal fat metabolism, oxidative stress, and insulin resistance are positively correlated with peroxidation and abnormal cytokine production. Recent studies have revealed that Solanum nigrum extracts (SNE) possess anti-inflammatory, antioxidation, antihyperlipidemia, and liver protection abilities. Therefore, the present study investigated the in vivo and in vitro effects of an SNE on nonalcoholic fatty liver (NAFL)-induced hepatitis. In vivo data demonstrated that the SNE reduced blood triglyceride, sugar, and cholesterol levels, as well as fat accumulation, oxidative stress, and lipid peroxidation in high-fat-diet-treated mice. The results indicated that the SNE downregulated the expression of fatty acid synthase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase), and sterol regulatory element-binding proteins (SREBPs) through the AMP-activated protein kinase (AMPK) pathway and upregulated the expression of carnitine palmitoyltransferase 1 (CPT1) and peroxisome proliferator-activated receptor alpha. Furthermore, we prepared a Solanum nigrum polyphenol extract (SNPE) from the SNE; the SNPE reduced hepatic lipid (oleic acid) accumulation. Therefore, SNE have the potential to alleviate NAFL-induced hepatitis, and polyphenolic compounds are the main components of SNE. Moreover, SNE can be used to develop health-food products for preventing NAFL disease.

Mulberry water extract regulates the osteoblast/osteoclast balance in an ovariectomic rat model.

Mulberry has favorable antioxidant ability. Menopause is a major cause of osteoporosis in women, and it is partially associated with oxidative stress. Here, mulberry water extract (MWE) was fed to ovariectomic (OVX) rats to explore the potential effect of MWE on osteoporosis. The results revealed that plasma alkaline phosphatase (ALP) significantly decreased in the OVX rats after MWE administration for 8 weeks. Histological examination showed that the MWE increased the density of trabecular bone in the OVX rats. It also revealed that the MWE increases the expression of Runx2 and decreases that of the receptor activator of nuclear factor κB and its ligand in the OVX rats. This implies that MWE might regulate osteoblast differentiation and osteoclast proliferation. The MWE improved the antioxidant status by lowering the expression of heme oxygenase-1. In addition, the MWE increased the expression of osteocalcin, ALP, and bone morphogenetic protein-2 in an osteoblast cell line, MG-63. The present results imply that MWE has potential to decelerate osteoporosis in an experimental OVX rat model.