Abstract
Adipose tissue secretes numerous hormone-like factors, which are known as adipokines. Adipokine receptors have been identified in the central nervous system but the potential role of adipokine signaling in neuroprotection is unclear. The aim of this study is to determine (1) Whether adipokines secreted from cultured adipose tissue of lean humans is protective against oxidative stress-induced neurotoxicity in human SH-SY5Y neuronal cells; and (2) To explore potential signaling pathways involved in these processes. Adipose tissue conditioned media (ATCM) from healthy lean subjects completely prevented H2O2 induced neurotoxicity, while this effect is lost after heating ATCM. ATCM activated the phosphorylation of ERK1/2, JNK and Akt at serine 308 in SH-SY5Y cells. PD98059 (25 µM), SP600125 (5 µM) and LY29400 (20 µM) partially blocked the protective effects of ATCM against H2O2 induced neurotoxicity. Findings demonstrate that heat-sensitive factors secreted from human adipose tissue of lean subjects are protective against H2O2 induced neurotoxicity and ERK1/2, JNK, and PI3K signaling pathways are involved in these processes. In conclusion, this study demonstrates preliminary but encouraging data to further support that adipose tissue secreted factors from lean human subjects might possess neuroprotective properties and unravel the specific roles of ERK1/2, JNK and PI3K in these processes.
Highlights
Alzheimer’s disease (AD) is the leading cause of dementia for people aged over 60
Adipose tissue conditioned media (ATCM) that had been heated to 95 °C for 10 min showed no protective effects against H2O2 induced neurotoxicity, suggesting that heat-sensitive factors secreted from human visceral adipose tissue protect against
Our current study demonstrates that heat-sensitive factors secreted from human adipose tissue of lean subjects are protective against H2O2 induced neurotoxicity and extracellular-signal-regulated kinases1/2 (ERK1/2), Jun N-terminal kinases (JNK), and PI3K signaling pathways are potentially involved in these processes
Summary
Alzheimer’s disease (AD) is the leading cause of dementia for people aged over 60. The global prevalence of dementia in this age group is predicted to double every 20 years, affecting more than 80 million people worldwide by 2040 [1]. Adipokine levels from individuals with obesity are altered when compared to lean counterparts with a general reduction in adiponectin and increase in leptin secretion [3]. Multiple adipokine receptors such as adiponectin receptor [4], leptin receptor [5] and resistin receptor [6] have been reported in the central nervous system (CNS). Chan et al [7] reported that adiponectin is protective against amyloid beta (Aβ) induced neurotoxicity in Sw-APP transfected SH-SY5Y cells under oxidative stress conditions. Whether secreted factors from adipose tissue holistically are involved in the pathogenesis or prevention of AD remains unknown
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