Ultraviolet (UV) light induces skin photoaging, which is characterized by thickening, wrinkling, pigmentation, and dryness. Astaxanthin (AST), a ketocarotenoid isolated from Haematococcus pluvialis, has been extensively studied owing to its possible effects on skin health as well as UV protection. In addition, AST attenuates the increased generation of reactive oxygen species (ROS) and capillary regression of the skeletal muscle. In this study, we investigated whether AST could protect against UV-induced photoaging and reduce capillary regression in the skin of HR-1 hairless mice. UV light induces wrinkle formation, epidermal thickening, and capillary regression in the dermis of HR-1 hairless mice. The administration of AST reduced the UV-induced wrinkle formation and skin thickening, and increased collagen fibers in the skin. AST supplementation also inhibited the generation of ROS, decreased wrinkle formation, reduced epidermal thickening, and increased the density of capillaries in the skin. We also found an inverse correlation between wrinkle formation and the density of capillaries. An association between photoaging and capillary regression in the skin was also observed. These results suggest that AST can protect against photoaging caused by UV irradiation and the inhibitory effects of AST on photoaging may be associated with the reduction of capillary regression in the skin.

Ultraviolet (UV) induces skin photoaging, which is characterized by thickening, wrinkling, pigmentation, and dryness. Astaxanthin, a ketocarotenoid from Haematococcus pluvialis, has been extensively studied with respect to its possible effect on skin health as well as UV protection. In addition, astaxanthin attenuates increases in the generation of reactive oxygen species (ROS) and capillary regression of skeletal muscle. In the present study, we investigated whether astaxanthin would protect UV-induced photoaging and capillary regression in the skin of HR-1 hairless mice. UV induces wrinkle formation, thickness and capillary regression in dermis of hairless mice and the administration of astaxanthin decreased the UV-induced wrinkle formation, skin thickness, and increase in collagen fibers in skin. Astaxanthin supplementation also inhibited the levels of ROS generation and attenuated the decreases in wrinkle formation, thickness and capillary number in the skin. We also found an inverse correlation between wrinkling and capillary number, and the photoaging associated with capillary regression in skin. These results suggest that astaxanthin can protect against photoaging caused by ultraviolet irradiation and the effects of astaxanthin in photoaging inhibition may be associated with the protection of capillary regression in skin.

Disuse condition leads to decrease fiber cross‐sectional area and satellite cell activity in skeletal muscle. Transcutaneous electrical stimulation (ES) can suppress unloading‐induced muscle atrophy, but not prevent. Lemon myrtle (LM), one of herbs, could activate muscle satellite cells in our previous study. Therefore, the preventive effects of the lemon myrtle supplementation on muscle atrophy were investigated. In addition, we determined the activation in muscle satellite cells, the number of myonuclei, and the prevention of disuse‐induced muscle atrophy by the combination of LM supplementation and ES. Wistar rats were divided into 5 groups; control (CON), hindlimb unloading (HU), HU + LM, HU + ES and HU + LM + ES groups. The experiment period was 14 days. Unloading condition resulted in a decrease in the fiber cross‐sectional area (FCSA). The FCSA was significantly increased in HU + LM + ES group than in the other three groups (HU, HU + LM and HU + ES). In addition, the expression levels of Pax 7, MyoD and myogenin were higher in HU + LM + ES group compared with the other three groups (HU, HU + LM and HU + ES). Furthermore, the number of myonuclei were significantly decreased in HU, HU + LM and HU + ES groups than in CON group although there was no significant difference between in HU + LM + ES group and CON group. These results suggest that the combination of lemon myrtle supplementation and electrical stimulation suppressed the reduction of the fiber cross‐sectional area compared with lemon myrtle supplementation or electrical stimulation alone, and these alterations were accompanied with an increase in the number of myonuclei associated with the activation of muscle satellite cells.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Cachexia is a complex metabolic syndrome associated with underlying chronic diseases and is characterized dysfunction of mitochondrial oxidative phosphorylation in skeletal muscle. The preventive effects of medium‐chain triglycerides (MCT) supplementation on the dysfunction of mitochondrial oxidative phosphorylation in skeletal muscle under cachectic condition have been investigated in the present study. ICR mice were randomly divided into 4 groups; control, lipopolysaccharide (LPS), LPS plus long‐chain triglycerides (LCT), LPS plus MCT supplementation. LCT and MCT oil (The Nisshin OilliO Group, Ltd, Tokyo, Japan) were administered to the LPS+LCT and LPS+MCT groups orally by a catheter for 1 week. Cachexia was induced in the LPS, LPS+LCT and LPS+MCT groups via LPS injection (7.5 mg/kg body weight, i.p.) after the supplementation. LPS resulted in a decrease in succinate dehydrogenase (SDH) activity, which is an indicator of mitochondrial function, and PGC‐1α, which is an indicator of mitochondrial biogenesis, in tibialis anterior muscles. LPS also induced a reduction of total ketone bodies concentration level in blood plasma. Meanwhile, MCT supplementation suppressed the decrease of SDH activity and total ketone bodies concentration. In addition, MCT supplementation increased the level of citrate synthase activity in the muscles. These results suggested that MCT supplementation could prevent dysfunction of mitochondrial oxidative phosphorylation in skeletal muscle under cachectic condition.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Hyperglycemia causes microvascular impairment in skeletal muscle of diabetes. Transcutaneous carbon dioxide (CO2) have been shown to increase capillary in skeletal muscle of healthy rats via the increase of angiogenic factor. The purpose of this study was to determine the effects of transcutaneous CO2 on muscle capillary impairment by exposure of hyperglycemia in streptozotocin (STZ)‐treated diabetic rats. Twenty‐four male Wistar rats (220~270g) were divided into control (CON), CO2, STZ and STZ+CO2 groups. STZ (50 mg/kg) was injected into the tail vein of rats. Blood glucose levels above 250 mg/dl after 2 days of the STZ injection confirmed the diabetic state. The lower limbs in rats were shaved and hydrogel was applied afterwards. The CO2 adaptor was attached to the limbs and sealed, and CO2 was administered into the adaptor for 30 min. This treatment was performed 5 days per week for 8 weeks. STZ resulted in capillary regression, indicated by decreases in capillary‐to‐fiber ratio. However, the capillary‐to‐fiber ratio in STZ + CO2 was higher than that in STZ. In addition, the protein expression level of vascular endothelial growth factor (VEGF), which is angiogenic factor, in STZ + CO2 was higher than that in STZ. The protein expression level of thrombospondin‐1 (TSP‐1), which is antiangiogenic factor, in STZ + CO2 was lower than that in STZ. These results indicated that transcutaneous CO2 attenuated the capillary regression via the increase of angiogenic factor and the decrease of antiangiogenic factor.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.