ZusammenfassungInflammaging bezeichnet einen chronischen Entzündungszustand, der durch altersbedingte Veränderungen des Immunsystems entsteht. Dieser wird als Grundlage vieler chronisch-entzündlicher Alterskrankheiten wie z.B. Arteriosklerose, Diabetes mellitus Typ 2, Morbus Alzheimer und Krebserkrankungen vermutet. Die Entstehung des vorherrschenden proinflammatorischen Milieus und der Verlauf des Entzündungsprozesses wird durch oxidativen Stress beschleunigt und in manchen Fällen verstärkt. Bei Entzündungsprozessen schütten aktivierte Immunzellen ein Arsenal an bioaktiven Stoffen aus, welche synergistisch zusammenwirken und neben positiven Wirkungen auch zu Zell- und Gewebeschäden führen. Im Fall einer manifesten Infektion sind ähnliche Prozesse beschrieben worden. Komplexe Phytotherapeutika (z.B. Padma 28) sind als pleiotrop wirkende Gemische geeignet, diesen krankmachenden Prozess an unterschiedlichen Wirkorten zu unterbinden. So sind etwa neben dem klinischen Effekt von Padma 28 bei Arteriosklerose auch verschiedene antiatherogene Wirkungsmechanismen des Präparats gut dokumentiert. Die Resultate stützen die Hypothese eines «multi- target»-Behandlungsansatzes von chronisch-entzündlichen Erkrankungen mit pflanzlichen Vielstoffgemischen, die hier einen wertvollen Betrag für neue Präventions- und Therapieverfahren liefern können. Sie sind somit geeignet, den Formenkreis von Inflammaging günstig zu beeinflussen, die Entstehung von Folgeerkrankheiten zu verlangsamen bzw. in manchen Fällen zu verhindern.

MDI 301 is a picolinic acid-substituted ester of 9-cis retinoic acid. It has been shown in the past that MDI 301 increases epidermal thickness, decreases matrix metalloproteinase (MMP) activity, and increases procollagen synthesis in organ-cultured human skin. Unlike all-trans retinoic acid (RA), MDI 301 does not induce expression of proinflammatory cytokines or induce expression of leukocyte adhesion molecules in human skin. In the present study we examined topical MDI 301 treatment for ability to improve the structure and function of skin in three models of skin damage in rodents and for ability to improve abrasion wound healing in these models. MDI 301 was applied daily to the skin of rats treated with the potent corticosteroid, clobetasol propionate, to the skin of diabetic rats (8 weeks posttreatment with streptozotocin) and to the skin of aged (14-16-month-old) rats. In all three models, subsequently induced abrasion wounds healed more rapidly in the retinoid-treated animals than in vehicle-treated controls. Immediately after complete wound closure, tissue from the wound site (as well as from a control site) was put into organ culture and maintained for 3 days. At the end of the incubation period, culture fluids were assessed for soluble type I collagen and for MMPs-2 and -9. In all three models, the level of type I collagen was increased and MMP levels were decreased by MDI 301. In all three models, skin irritation during the retinoid-treatment phase was virtually nonexistent.

Low molecular weight antioxidants (LMWA) supplements are a popular and routine approach to assist the cell and the whole organism to cope with increasing oxidative stress. Numerous experiments have been conducted in which exogenous antioxidants were supplemented to cells, animals and humans to prevent and delay pathological disorders associated with reactive oxygen species. Recently, many meta-analysis publications have demonstrated the failure of this approach and in some cases even showed an increase in the severity of the disease and all-cause mortality. The reasons for the lack of success are not fully understood and the concept of antioxidant therapy is questionable. We suggest a new explanation concerning the way antioxidants function in the living cells that can elucidate some of the conflicting data published. The aim of this study was to examine the hypothesis that the overall antioxidant capacities of cells in culture remains constant and since the cells tightly regulate this antioxidant network, supplementation with exogenous antioxidants cannot enhance the total antioxidant capacity of the cells. This assumption was examined in HaCaT, Hep3B, PC3 and Caco-2 cells using several types of antioxidant supplements. It has been shown that while the levels of the specific administrated antioxidant increased significantly intracellularly, the overall antioxidant capacity of the cells as evaluated by various methods did not increase, and in some cases, even decreased. These results support the hypothesis and demonstrate that the total antioxidant capacity of these cells in culture is kept under tight regulation and cannot be enhanced by exogenous LMWA.

The present view focuses on the possibility that cationic antimicrobial peptides (CAMPs) might, in addition to their killing effects due to permeabilization of microbial membranes, also function similarly to beta-lactam antibiotics to activate nascent autolytic wall enzymes, leading to bacteriolysis. Since the massive release of microbial cell wall components is a major cause of postinfectious sequelae, the in vivo process of bacteriolysis must be controlled. Due to the emergence of antibiotic resistance in pathogenic bacteria, CAMPs might be useful as an alternative to antibiotics. However, they should be used with caution, since they might also function as a 'double-edged sword' by injuring both the bacteria and host.