Dietary schizophyllan reduces mitochondrial damage by activating SIRT3 in mice.

Schizophyllan (SPG), produced by Schizophyllum commune, is an exopolysaccharide with multiple academic and commercial uses, including in the food industry and for various medical functions. We previously demonstrated that SPG conjugated with c-Src peptide exerted a significant therapeutic effect on mouse models of the acute inflammatory diseases polymicrobial sepsis and ulcerative colitis. Here we extended these results by investigating whether SPG exerted a protective effect against mitochondrial damage in the liver via sirtuin 3 (SIRT3) induction, focusing on the deacetylation of succinate dehydrogenase A (SDHA) and superoxide dismutase 2 (SOD2). Liver damage models induced by alcohol or conjugated linoleic acid (CLA, which simulates lipodystrophy) in SIRT3-/-, SOD2-/-, and SDHA-/- mice were used. Results showed that dietary supplementation with SPG induced SIRT3 activation; this was involved in mitochondrial metabolic resuscitation that countered the adverse effects of alcoholic liver disease and CLA-induced damage. The mitochondrial SIRT3 mediated the deacetylation and activation of SOD2 in the liver and SDHA in adipose tissues, suggesting that SPG supplementation reduced ethanol-induced liver damage and CLA-induced adverse dietary effects via SIRT3-SOD2 and SIRT3-SDHA signaling, respectively. Together, these results suggest that dietary SPG has a previously unrecognized role in SIRT3-mediated mitochondrial metabolic resuscitation during mitochondria-related diseases.

[Influence of schizophyllan, streptomycin and rifampicin on histopathological changes in mice infected with tubercle bacilli (author's transl)].

Experimental tuberculosis in mice infected with streptomycin-resistant Mycobacterium tuberculosis SCHACHT strain was treated with streptomycin or rifampicin alone and in combination with schizophyllan. The histopathogical tests of various organs of the treated mice were carried out. 1) In the group of mice treated with streptomycin alone, the moderate focal proliferation of RE cells were seen at the beginning of infection. However, durable activation of RE cells and the prolongation of life-span could not be recognized as compared with control animals. 2) The treatment with streptomycin-schizophyllan combination appeared to be somewhat more effective than schizophyllan alone, the phagocytic capacity being more strongly stimulated. 3) In the group treated with rifampicin alone, the therapeutic effect could be exhibited by the direct antibacterial action of rifampicin, but the activation of RE cells was slight. When rifampicin was discontinued, the growth of tubercle bacilli was rapidly resumed, and the durable therapeutic effect seemed not to be expected. Degeneration of hepatic cells tended to develop. 4) In the group treated with rifampicin-schizophyllan combination, the antibacterial effect of rifampicin appeared to be potentiated by the strong activation of RE cells by schizophyllan, showing the durable therapeutic effects.