Objective Sympathetic neuronal activity in the thymus and lymph nodes is differentially regulated during reproductive aging. The aim was to investigate the role of estrogen on sympathetic neuronal expression in the thymus and mesenteric lymph nodes of early middle-aged ovariectomized female rats implanted with 17b-estradiol pellets. Methods 17b-Estradiol pellets (0.6 and 300) were implanted subcutaneously in ovariectomized middle-aged female Sprague-Dawley rats (n = 8/group) for a period of 30 days. At the end of the treatment period, the thymus and mesenteric lymph nodes were isolated and analyzed for the expression of tyrosine hydroxylase, nerve growth factor, and p-ERK, p-CREB and p-Akt. Results The age-related increase in tyrosine hydroxylase expression in the thymus was abrogated by ovariectomy, while estrogen suppressed it further and nerve growth factor expression was altered based on the dose of estrogen. In contrast, estrogen increased tyrosine hydroxylase and nerve growth factor expression in the mesenteric lymph nodes. Estrogen enhanced p-ERK/ total ERK, CREB/total CREB and p-Akt/total Akt expression in a dose-dependent manner. Free radical generation was augmented by estrogen in the thymus alone. Conclusions These results suggest that estrogen differentially influences sympathetic neuronal activity in the primary and secondary lymphoid organs to influence immunity.

AbstractBackgroundVirgin coconut oil (VCO), a cold processed form of coconut oil, is traditionally consumed in Asian countries owing to its nutritional and medicinal properties. The aim of this study was to investigate whether the health benefits of VCO involve alterations in immune responses that are regulated by intracellular signaling molecules in the spleens of rats.MethodsYoung male Wistar rats were fed with three doses of VCO in diet for 30 days. At the end of the treatment period, spleens were isolated and in vitro effects on immune responses (Concanavalin A [Con A]-induced lymphoproliferation and cytokine production), and direct effects of VCO treatment on intracellular signaling molecules and antioxidant status were examined. Serum was collected to measure glucose, lipid levels, and leptin.ResultsVCO supplementation in diet enhanced Con A-induced splenocyte proliferation and Th1 cytokine production while it suppressed the proinflammatory cytokine production. VCO increased the expression of mechanistic target of rapamycin (p-mTOR), sirtuin1 (SIRT1), liver kinase B1 (p-LKB1) p-ERK, and p-CREB in spleen. Similarly, VCO increased the activities of antioxidant enzymes while it suppressed lipid peroxidation in the spleen. VCO diet had hypolipidemic effects on the rats: an increase in high density lipoprotein cholesterol (HDL-C) levels while lowering triacylglycerol (TAG) levels.ConclusionThe health benefits of VCO may be mediated through enhanced Th1 immunity through the upregulation of survival signaling pathways and inhibition of free radical generation in the spleen besides its capacity to induce hypolipidemia.

Objective Virgin coconut oil (VCO) is used as a traditional medicine in Asian countries because of its therapeutic effects mediated through hypolipidemic, antimicrobial and anti-oxidant properties. The interactions between the sympathetic noradrenergic nervous system and the immune cells of the lymphoid organs (thymus and lymph nodes) modulate immunity to determine health or onset of inflammatory diseases. The aim of the present study was to investigate the role of VCO in modulating neuronal and anti-inflammatory factors in the thymus and mesenteric lymph nodes (MLN). Methods Young male Wistar rats (n = 8/group) were fed with a control diet or diet supplemented with 4%, 8%, and 16% of VCO. After a 30-day treatment period, thymus and MLN were isolated to analyze the expressions of p-tyrosine hydroxylase, nerve growth factor, p-nuclear factor-jB (p50 and p65), p-mechanistic target of rapamycin, SIRT1, p-LKB1 and intracellular signaling molecules (p-ERK, p-Akt, p-CREB). Activities of anti-oxidant enzymes and the extent of lipid peroxidation were also analyzed. Results In the thymus, a VCO diet enhanced the expression of p-tyrosine hydroxylase, nerve growth factor and SIRT1, and the activities of anti-oxidant enzymes, whereas it decreased the expression of p-nuclear factor-jB (p50 and p65) and the extent of lipid peroxidation. In the MLN, VCO augmented the expression of p-tyrosine hydroxylase, nerve growth factor, pmechanistic target of rapamycin, SIRT1 and p-LKB1, and activities of anti-oxidant enzymes, whereas p-nuclear factor-jB (p50 and p65) expression was inhibited. VCO enhanced the expression of intracellular signaling molecules in both the thymus and MLN. Conclusion Dietary VCO might modulate immune responses by upregulating neuroprotective factors, and suppressing inflammatory mediators and oxidative stress through intracellular signaling pathways.