EA improved the reproductive functions, decreased body weight and improved experimental depressive behaviour. The PCOS rats presented with reproductive dysfunctions such as lack of regular oestrous cyclicity, metabolic disorders such as increased body weight and insulin resistance, and depression and anxiety-like behaviours. We examined the reproductive, metabolic and behavioural phenotypes, validated the effect of EA, and explored the role of hypothalamic DNA methylation by analysing the methylation of global DNA and selected candidate genes. Rats were randomly divided into four groups - controls, diet-induced obesity, PCOS and PCOS+EA. In the present study, we used the 5 alpha-dihydrotestosterone-induced PCOS-like rat model and treated the rats with electro-acupuncture (EA). Recently, epigenetic studies focusing on DNA methylation in PCOS have received much attention, but the mechanisms are still unclear. Polycystic ovary syndrome (PCOS) is a common reproductive and endocrine disease of unknown aetiology. Pyrosequencing showed that the DNA methylation of some PCOS candidate genes was changed in the PCOS and PCOS+EA groups, suggesting that hypothalamic DNA methylation plays an important role in the development of PCOS and in mediating the effects of electro-acupuncture treatment. What is the main finding and its importance?Global DNA methylation and expression of DNA methyltransferases (DNMTs) were increased in PCOS-like rats, and electro-acupuncture (EA) decreased global DNA methylation and DNMT3b expression. What is the central question of this study?What is the role of hypothalamic DNA methylation in the development of polycystic ovary syndrome (PCOS) and the response to electro-acupuncture treatment. Altogether, our findings identify p38 alpha MAPK as a novel regulator of muscle atrophy and suggest that the suppression of intracellular signaling mediated by p38 alpha MAPK serves as a potential target for the treatment of muscle atrophy. We also identified CAMK2B as a potential downstream target of p38 alpha MAPK and found that the pharmacological inhibition of CAMK2B activity suppresses denervation-induced muscle atrophy. Compared with the control mice, these mutant mice are significantly resistant to denervation-induced muscle atrophy, suggesting that p38 alpha MAPK positively regulates muscle atrophy. In the present study, we generated a mutant line in which p38 alpha MAPK is specifically abrogated in muscle tissues. p38 alpha mitogen-activated protein kinase (p38 alpha MAPK) is a ubiquitous signaling molecule that is implicated in various cellular functions, including cell proliferation, differentiation, and senescence. Therefore, the demand to further understand the pathology of muscle atrophy and establish a treatment modality for patients with muscle atrophy is significant. However, only a few therapeutic interventions leading to marginal clinical benefits in patients with this condition are currently available. The loss of skeletal muscle mass is a major cause of falls and fractures in the elderly, leading to compromised independence and a decrease in the quality of life. ![]() Recombinant Alpaca Anti-Rabbit IgG monoclonal antibody, clone WII1355 Īnti-Rabbit IgG Fc polyclonal antibody Īnti-Rabbit IgG + IgM polyclonal antibody Īnti-Rabbit IgG polyclonal antibody ![]() Recombinant Alpaca Anti-Rabbit IgG Fc monoclonal antibody, clone IB21
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