Effect of long-term administration of cordycepin from Cordyceps militaris on testicular function in middle-aged rats.

This study was carried out to examine the potential beneficial effect of cordycepin on the decline of testicular function induced with age. A total of 30 male Sprague-Dawley rats (twenty-four 12-month-olds and six 2-month-olds) were divided into five groups. The young control (YC) and middle-aged control (MC) groups received vehicle only. Cordycepin-treated groups were administered daily doses of oral cordycepin at 5, 10, and 20 mg/kg body weight for 4 months. As a result, the MC group exhibited epididymal weight loss, decreased sperm motility, and reduced spermatogenesis compared to the young control group. Interestingly, the epididymal weights of middle-aged rats were dose-dependently increased by treatment with cordycepin. Cordycepin also improved calcium levels and decreased urea and nitrogen, uric acid, and creatinine in the blood of middle-aged rats. In addition, cordycepin significantly increased sperm motility and the progressiveness of sperm movement. All cordycepin-treated groups showed well-arranged spermatogonia, densely packed cellular material, and increased numbers of mature spermatozoa in the seminiferous lumen compared to the middle-aged control group. These results indicate that long-term administration of cordycepin can counteract the decline of testicular function in middle-aged rats.

Dietary ß-glucan regulates the levels of inflammatory factors, inflammatory cytokines, and immunoglobulins in interleukin-10 knockout mice.

ß-Glucan is known to have anti-inflammatory properties, and several studies have demonstrated the beneficial effects of dietary ß-glucan on inflammatory bowel disease (IBD). However, it is unknown how ß-glucan mediates its protective effects on IBD. Therefore, we used a well-established mouse model for IBD, interleukin (IL)-10(-/-) mice, to explore the protective effects of ß-glucan on IBD-like symptoms caused by IL-10 deficiency. The mice were divided into two groups: IL-10(-/-) and IL-10(-/-) + ß-glucan treatment groups. IL-10(-/-) mice treated with dietary ß-glucan exhibited less inflammation within the colon. The levels of immunoglobulins A and E were lower in the serum, spleen, mesenteric lymph nodes, and Peyer's patches in the IL-10(-/-) mice compared with the IL-10(-/-) + ß-glucan mice. Also, the expression of pro-inflammatory cytokines was lower in the IL-10(-/-) + ß-glucan mice compared with the IL-10(-/-) mice. Histological analysis also revealed that administration of dietary ß-glucan in IL-10(-/-) mice reduced colonic tissue damage. Finally, the expression of the pro-inflammatory cytokine tissue necrosis factor-α was significantly lower with dietary ß-glucan treatment in IL-10(-/-) mice. In conclusion, dietary ß-glucan reduces the inflammation associated with IBD caused by IL-10 deficiency.

Dietary pectin regulates the levels of inflammatory cytokines and immunoglobulins in interleukin-10 knockout mice.

Pectin has protective, anti-inflammatory effects on inflammatory bowel disease (IBD), but the exact mechanism is unknown. Therefore, we investigated the immunological effect of dietary pectin in IL-10(-/-) mice, a murine model for IBD. Cytokine expression, CD4(+) and CD8(+) T cell populations, and immunoglobulin secretion were observed in three groups of mice: normal (BALb/c), IL-10(-/-), and IL-10(-/-) treated with pectin. Pectin treatment reduced expression of TNF-α and GATA-3, an important transcription factor for the Th2 immune response. These mice also expressed lower levels of IgE in the spleen and Peyer's patches (PP) and lower IgG and IgM expression in PP. Interestingly, IL-10 deficiency resulted in lower CD4(+) and CD8(+) populations in the spleen, mesenteric lymph node (MLN), and PP; however, pectin counteracted these declines in the MLN and PP. Therefore, dietary pectin downregulates the inflammatory response in the colon by moderating the production of proinflammatory cytokines and immunoglobulins.