PO-109 Resistance Training prevents Skeletal Muscle Atrophy Induced by hypoxia through regulating Akt-FoxO1 pathway

Objective Skeletal muscle atrophy induced by hypoxia on the plateau will lead to the decrease of muscle strength and the degeneration of athletic ability. Resistance training is an efficient method to stimulate the growth of muscle and improve protein synthesis. Akt-FoxO1 (Fork head box protein 1) pathway plays a significant role in the regulation of skeletal muscle protein degradation. However, it is not clear whether resistance training could prevent skeletal muscle atrophy induced by hypoxia and what is the regulation role of Akt-FoxO1 pathway. This study built a rat model that resistance training inhibited the skeletal muscle atrophy induced by hypoxia and explore the variation of Akt, FoxO1, Murf and Atrogin-1. Methods 40 male 8-week-old Sprague-Dawley (SD) rats were divided into 4 groups randomly: control group (C), resistance training group (R), hypoxia group (H) and hypoxia resistance training group (HR). H and HR group were placed into simulated 4000m altitude (12.4%, O2%) and R and HR group received ladder resistance training. Their incremental load is calculated by using average body weight. After 4 weeks intervention of hypoxia and resistance training, body composition, wet weight of skeletal muscle (soleus, musculus gastrocnemius,extensor digitorum longus and muscelus biceps brachii) and skeletal muscle cross-sectional area (CSA) were measured. The expression of Akt, FoxO1, Murf and Atrogin-1 were detected by Western blot and RT-PCR.Moreover,immunofluorescence technique was used to locate the phosphorylation of FoxO1. Results The lean body mass of HR group was significantly higher than H group (P<0.05). The wet weight and CSA of muscelus biceps brachii in HR group were also higher than H group obviously (P<0.05). The results of real-time fluorescence quantitative PCR and western blot showed that the expression of FoxO1 and MuRF of hypoxia group (H group) were significantly higher than control group. However after the intervention of resistance training, the expression of Akt was significantly up-regulate and FoxO1, MuRF were significantly down-regulate. Immunofluorescence technique was used to observe the location of FoxO1 phosphorylation and the expression out of nucleus. Conclusions Resistance training contribute to prevent the occurrence of skeletal muscle atrophy induced by hypoxia and the form of climbing ladder training can stimulate the hypertrophy of biceps in rats. The results revealed that FoxO1 phosphorylation out of nucleus became higher after resistance training. All above revealed that resistance training could inhibit skeletal muscle atrophy induced by hypoxia. Akt promoted FoxO1 phosphorylation may become the molecular mechanisms that resistance training can inhibit the atrophy of skeletal muscle induced by hypoxia.

Presence of anti-Leishmania spp. antibodies in slaughter horses in Brazil

The objective of this study was to investigate the presence of anti-Leishmania spp. antibodies using an indirect immunofluorescence technique in the serum of equidae slaughtered in two slaughterhouses registered with the Federal Inspection Service. Titers greater than 40 were considered reagents. Blood samples were collected from 398 animals of both sexes, with different ages, and coming from six Brazilian states, of which 46.0% (183/398) were reactive, indicating that these animals were exposed to the leishmaniasis agent that is widely distributed in Brazil.

Langerhans Cells Express IL-17A in the Epidermis of Chromoblastomycosis Lesions

Chromoblastomycosis (CBM) is a chronic fungal infection that affects skin and subcutaneous tissue, and little is known about the immunological aspects of such lesions. We have previously described the high expression of IL-17 in this group. Understanding the innate immune response of patients with CBM would improve the knowledge of its immunopathogenesis and contribute to the most appropriate therapies. Nineteen biopsies of verrucous form were obtained from patients with clinical and histopathological diagnosis of CBM, without treatment. This was done with a double immunostaining with conventional immunohistochemistry and immunofluorescence technique as well as confocal microscopy to detect Langerin and IL-17 expression. All of the specimens that were analyzed showed expression of Langerin in the epidermis - the same as the control group. However, only the CBM group presented cells expressing CD207 in the dermis. Interestingly, the coexpression of IL-17 and Langerin was visualized along the epidermis and dermis in 100% of the lesion group. We demonstrated for the first time in situ coexpression of IL-17 and Langerin (CD207) in epidermal cells of patients with CBM and speculated on their role as IL-17-producing cells or whether they could be a new subpopulation of dendritic cells distinct from Langerhans cells.