Placenta extracts are used for their health benefits; however, the anti-fatigue effects of placenta have not been elucidated. Thus, we investigated the anti-fatigue effects of porcine placenta extract (PE) and the amino acids present in the PE (glycine, Gly; proline, Pro; glutamic acid, GA; and arginine, Arg) using a forced swimming test (FST) and a tail-suspension test (TST) on mice. Whole PE or individual amino acids decreased immobility times in the FST. PE, Pro, and Arg all lowered blood levels of lactic acid and alanine aminotransferase (ALT). PE and Gly improved glycogen content and catalase activity. As determined from the serum after the FST: PE regulated the effects of interferon (IFN)-γ and tumor necrosis factor (TNF)-α; GA regulated the effects of IFN-γ; Gly and Arg regulated the effects of interleukin (IL)-6; and all of the amino acids present in PE regulated the effects of TNF-α. As determined from the spleen after the FST: Gly and Arg regulated the effects of IL-1β; Gly, Pro, and Arg regulated the effects of IL-6; PE and all of the amino acids present in PE regulated the effects of TNF-α. After the TST, PE and all of the amino acids present in PE reduced immobility duration as well as levels of aspartate aminotransferase and ALT. As determined from the serum after the TST: PE and Gly regulated the effects of TNF-α; Gly and Arg regulated the effects of IL-1β; Gly, Pro, and Arg regulated the effects of IL-6; PE and all of the amino acids present in PE regulated the effects of TNF-α. These results suggest that PE should be considered a candidate anti-fatigue agent.

Gomisin A (GA), a lignan component contained in the fruit of Schisandra chinensis Baillon, improves hepatic cell degeneration, vasodilatory activity and insulin sensitivity. These effects also impact the immune system, including various inflammatory mediators and cytokines. In this study, the anti-inflammatory effect of GA on lipopolysaccharide-stimulated mouse peritoneal macrophages was studied. Pretreatment with GA attenuated the expression of receptor-interacting protein 2 (RIP2) and IκB kinase-β (IKK-β) as well as IKK-β phosphorylation. The activation of nuclear factor-kappa B (NF-κB) in the nucleus, the phosphorylation of IκBα and degradation of IκBα in the cytosol were suppressed by GA. GA decreased the production and mRNA expression of the inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. In addition, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and production of nitric oxide were decreased by pretreatment with GA. In conclusion, these results show that the anti-inflammatory properties of GA potentially result from the inhibition of COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation. These results impact the development of potential health products for preventing and treating inflammatory diseases.

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Auditory dysfunction is related to large/small vessel occlusions and hemorrhage. Sudden sensorineural hearing loss (SSNHL) frequently occurs with anterior inferior cerebellar artery occlusion proximal to the internal auditory artery. Moreover, SSNHL has various pathogenetic mechanisms, the main proposed mechanisms being vascular disease, membrane ruptures, infection, and autoimmunity. Tumor necrosis factor (TNF) is an important cytokine in the inflammation process of cerebrovascular diseases. In the current study, the possible effects of polymorphisms in TNF-alpha and TNF-beta genes on SSNHL are evaluated. Two genetic polymorphisms in the TNF locus (TNF-alpha -308 G - ->A and TNF-beta +252 A - ->G) were investigated as risk factors for SSNHL by determining their prevalence in 97 SSNHL patients and in 587 controls. A significant increase was found for the TNF-beta allele 1 in SSNHL patients compared with the controls (chi( 2) = 7.251, P = .007, odds ratio [OR] = 1.534, confidence interval [CI] = 1.12-2.10). These findings suggest that the TNF-beta +252 locus plays an important role in the etiopathogenesis of SSNHL.