The world is facing the new challenges of an aging population, and understanding the process of aging has therefore become one of the most important global concerns. Sarcopenia is a condition which is defined by the gradual loss of skeletal muscle mass and function with age. In research and clinical practice, sarcopenia is recognized as a component of geriatric disease and is a current target for drug development. In this review we define this condition and provide an overview of current therapeutic approaches. We further highlight recent findings that describe key pathophysiological phenotypes of this condition, including alterations in muscle fiber types, mitochondrial function, nicotinamide adenine dinucleotide (NAD⁺) metabolism, myokines, and gut microbiota, in aged muscle compared to young muscle or healthy aged muscle. The last part of this review examines new therapeutic avenues for promising treatment targets. There is still no accepted therapy for sarcopenia in humans. Here we provide a brief review of the current state of research derived from various mouse models or human samples that provide novel routes for the development of effective therapeutics to maintain muscle health during aging.

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Nowadays, the exploration of zinc oxide nanoparticles (ZnO NPs) based products is booming in the various directions of bio-nanomedicine and other consumer products, but the comprehensive toxicological impact posed by ZnO NPs still remains unclear. The present study systematically investigates and correlates the toxicity evaluation of ZnO NPs in RAW 264.7 murine macrophages (in vitro) and male ICR mice (in vivo) by two different administration routes, i.e. g.i. and i.p. at different doses. The in vitro studies showed a slight rise in intracellular reactive oxygen species level (ROS), NF-kB transcription factor expression (TF) and NPs uptake at higher dose, indicating the non-toxic nature of ZnO NPs below 100 mg mL À1 doses. The in vivo results demonstrate a slight gain in body weight (BW), reduction in the organ weight, mild to severe pathological alteration in the organs depending upon NP dosage and mode of administration routes. The histopathological investigation suggests that the liver, kidney, lung, spleen, and pancreas may be the target organs for ZnO NPs according to the administration routes. Serum biochemistry assay shows an elevation in the GPT and ALP level, suggesting liver dysfunction. To our knowledge, this is the first study to report the toxic effects of ZnO NPs through i.p. administration.Further, the present work will offer a deeper understanding regarding the toxicology and in vivo behaviours of ZnO NPs in mice depending upon the various administration routes. † Electronic supplementary information (ESI) available: Supplementary Fig. 1 shows the TEM images of (A) bare ZnO NPs, (B) aminated ZnO NPs showing a thin lm coated on the ZnO surfaces, and (C) the surface charges of the bare and aminated ZnO NPs in aqueous solution at different pH measured by zeta potentiometer. Supplementary Fig. 2 shows the cellular uptake behavior of ZnO NPs. Supplementary Fig.3 shows the gross observation of mice aer intraperitoneal administration of 100 mg mL À1 ZnO nanoparticles. See

A natural compound C23 H32 O4 Cl, ascochlorin (ASC) isolated from an incomplete fungus, Ascochyta viciae has been known to have several biological activities as an antibiotic, antifungal, anti-cancer, anti-hypolipidemic, and anti-hypertension agent. In this study, anti-inflammatory activity has been investigated in lipopolysaccharide (LPS)-induced murine macrophage RAW 264.7 cells, since ASC has not been observed on the inflammatory events. The present study has clearly shown that ASC (1-50 μM) significantly suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2 ) and decreased the gene expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner. Moreover, ASC inhibited the mRNA expression and the protein secretion of interleukin (IL)-1β and IL-6 but not tumor necrosis factor (TNF)-α in LPS-stimulated RAW 264.7 macrophage cells. In addition, ASC suppressed nuclear translocation and DNA binding affinity of nuclear factor-κB (NF-κB). Furthermore, ASC down-regulated phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2) and p-p38. These results demonstrate that ASC exhibits anti-inflammatory effects in RAW 264.7 macrophage cells.

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