Osteoblasts are an important key factor for the pathogenesis of several bone-related diseases, notably in osteoporosis. Osteoporosis is a disorder categorized based on the bone mineral density (BMD) and an alteration in the bone micro-architecture had been considered as the major determinant for increasing the fracture risk. The available medicine for curing the osteoporosis shows a minimal or no activity against the genesis or function of osteoblasts. The present study was conducted to determine the influence of phyto Angelica species (Ang.) mediated synthesized copper quantum dots decorated chitosan on human osteoblast cells for application of osteoporosis. The phyto compound of Angelica sp. was extracted by ethanol as solvent and it has been characterized through spectral analyses. An Angelica sp. mediated synthesized copper oxide quantum dots (CuO QDs) and the presence of CuO QDs on chitosan have been analyzed and exhibited by important spectral investigations. The morphological observation of CuO QDs on the chitosan (CS) was visualized by the microscopic analyses. The MTT assay results showed that cell growth of CuO QDs/CS-Ang. by the concentration dependent. The highest cell growth (87%) was noted at 5 μg/mL followed by 80 and 77% at 15 and 25 μg/mL respectively. The functional groups and potential compounds of Angelica sp. with CuO QDs/CS has been improved the osteoblast cell activity as prophylactic potentials against osteoporosis.

Osteoporosis (OP) and increased fracture risk are widely observed comorbidities in chronic inflammatory rheumatic diseases (CIRDs). Improved knowledge of the immune/inflammatory pathways, which characterise the pathophysiology of rheumatoid arthritis (RA) and seronegative spondyloarthropathies (SpA), such as ankylosing spondylitis (AS) and psoriatic arthritis (PsA), have provided the link between inflammation and bone loss, via a complex network of bone cells, T and B cells, pro-inflammatory cytokines such as TNF-α, IL1, IL6, IL17, IL23, costimulator molecules, signalling pathways including both RANKL/RANK/OPG and Wnt signallings. The complex osteoimmunologic network in CIRDs suggested that the powerful anti-inflammatory activity of biologic drugs, beyond the control of the disease, was likely to reduce OP and fracture risk. In this respect, the available data deriving from clinical and experimental studies, conducted with TNF-α, IL6 and IL1 blockers, and B and T cell therapies, have demonstrated a beneficial effect on bone mineral density (BMD) and/or bone turnover markers (BTs). However, whether these drugs are able to positively influence also fracture risk has not yet been established, since the data available are sparse and inconclusive. Thus, systemic bone loss and increased fracture rates still remain relevant comorbidities that should be considered for screening and prevention, and proper treatment of patients with CIRDs despite the biologic therapy.

Loganin, a major iridoid glycoside obtained from fruits of Cornus officinalis, possesses anti-inflammatory, antitumor, antidiabetic, and osteoporosis prevention effects. Loganin has been linked to neuroprotection in several models of neurodegeneration, including Parkinson's disease (PD). However, mechanisms underlying the neuroprotective effects of loganin are still mostly unknown. Here, we demonstrated the protective effects of loganin against PD mimetic toxin 1-methyl-4-phenylpyridinium (MPP+ ) and the important roles of insulin-like growth factor 1 receptor (IGF-1R) and glucagon-like peptide 1 receptor (GLP-1R) in the neuroprotective mechanisms of loganin. In primary mesencephalic neuronal cultures treated with or without MPP+ , loganin up-regulated expressions of neurotrophic signals including IGF-1R, GLP-1R, p-Akt, BDNF, and tyrosine hydroxylase. Loganin protected against MPP+ -induced apoptosis by up-regulating antiapoptotic protein and down-regulating proapoptotic protein. Moreover, loganin attenuated MPP+ -induced neurite damage via up-regulation of GAP43 and down-regulation of membrane-RhoA/ROCK2/p-LIMK/p-cofilin. Loganin also attenuated MPP+ -induced reactive oxygen species (ROS) production. However, both AG1024, an IGF-1R antagonist, and exendin 9-39, a GLP-1R antagonist, attenuated the protective effects of loganin on MPP+ -induced cytotoxicity, apoptosis, neurite length decrease, and ROS production. Our results suggest that loganin attenuates MPP+ -induced apoptotic death, neurite damage, and oxidative stress through enhancement of neurotrophic signaling, activation of IGF-1R/GLP-1R, and inhibition of RhoA/ROCK pathway, providing the evidence that loganin possesses novel neuroprotective effects.

Vacuolar ATPases (V-ATPases) play a critical role in regulating extracellular acidification of osteoclasts and bone resorption. The deficiencies of subunit a3 and d2 of V-ATPases result in increased bone density in humans and mice. One of the traditional drug design strategies in treating osteoporosis is the use of subunit a3 inhibitor. Recent findings connect subunits H and G1 with decreased bone density. Given the controversial effects of ATPase subunits on bone density, there is a critical need to review the subunits of V-ATPase in osteoclasts and their functions in regulating osteoclasts and bone remodeling. In this review, we comprehensively address the following areas: information about all V-ATPase subunits and their isoforms; summary of V-ATPase subunits associated with human genetic diseases; V-ATPase subunits and osteopetrosis/osteoporosis; screening of all V-ATPase subunits variants in GEFOS data and in-house data; spectrum of V-ATPase subunits during osteoclastogenesis; direct and indirect roles of subunits of V-ATPases in osteoclasts; V-ATPase-associated signaling pathways in osteoclasts; interactions among V-ATPase subunits in osteoclasts; osteoclast-specific V-ATPase inhibitors; perspective of future inhibitors or activators targeting V-ATPase subunits in the treatment of osteoporosis.

When homeostatic regulatory systems are unable to maintain a normal serum sodium concentration, the organism must adapt to demands of a disordered internal environment, a process known as "allostasis." Human cells respond to osmotic stress created by an abnormal serum sodium level with the same adaptations used by invertebrate organisms that do not regulate body fluid osmolality. To avoid intolerable changes in their volume, cells export organic osmolytes when exposed to a low serum sodium concentration and accumulate these intracellular solutes when serum sodium concentration increases. The brain's adaptation to severe hyponatremia (serum sodium < 120 mEq/L) has been studied extensively. However, adaptive responses occur with less severe hyponatremia and other tissues are affected; the consequences of these adaptations are incompletely understood. Recent epidemiologic studies have shown that mild (sodium, 130-135 mEq/L) and moderate (sodium, 121-129 mEq/L) chronic hyponatremia, long thought to be inconsequential, is associated with adverse outcomes. Adaptations of the heart, bone, brain, and (possibly) immune system to sustained mild to moderate hyponatremia may adversely affect their function and potentially the organism's survival. This review explores what is known about the consequences of mild to moderate chronic hyponatremia and the potential benefits of treating this condition.

This corrects the article on p. 750 in vol. 46, PMID: 16385649.

This corrects the article on p. 751 in vol. 44, PMID: 14584089.