Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 3

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
In the current study, potential involvement of anthocyanins in the defence of the Zn hyperaccumulator plant, Noccaea caerulescens, was investigated in two independent glasshouse experiments. Plants were grown in compost amended with a range of Zn concentrations. In the first experiment, foliar herbivory was simulated by clipping the shoots with scissors, whilst in second experiment, plants were subjected to natural herbivory by thrips (Frankliniella occidentalis). In both experiments, foliar Zn concentrations were approximately twice as high as that applied to the soil, indicating accumulation occurred. In the clipping experiment, foliar anthocyanin concentrations decreased by 22–45 % with increasing soil Zn amendments and clipping increased anthocyanin concentrations by 17–24 % relative to unclipped plants. In a thrips feeding experiment, Zn treatment had little effect on anthocyanin content although there was a trend towards increased anthocyanin production in plants grown at the lower concentrations of Zn. Anthocyanin concentration increased by 49–52 % in N. caerulescens leaves subjected to thrip attack compared to that of thrip-free shoots. Thus, anthocyanins increased as a result of foliar damage (manual clipping and natural herbivory) and generally decreased with enhanced Zn concentrations. Foliar glucosinolate concentrations were higher in ungrazed leaves than in grazed leaves of the same thrip-infested plants, whilst anthocyanin production was higher in the grazed leaves. The possibility of an interaction between glucosinolate and anthocyanin production resulting from herbivory is discussed.
In ischemic stroke, the necrotic core is surrounded by a zone of infl ammation, in which delayed cell death aggravates the initial insult. Here, we provide evidence that the receptor for advanced glycation end products (RAGE) functions as a sensor of necrotic cell death and contributes to infl ammation and ischemic brain damage. The RAGE ligand high mobility group box 1 (HMGB1) was elevated in serum of stroke patients and was released from ischemic brain tissue in a mouse model of cerebral ischemia. A neutralizing anti-HMGB1 antibody and HMGB1 box A, an antagonist of HMGB1 at the receptor RAGE, ameliorated ischemic brain damage. Interestingly, genetic RAGE defi ciency and the decoy receptor soluble RAGE (sRAGE) reduced the infarct size. In vitro, expression of RAGE in (micro)glial cells mediated the toxic effect of HMGB1. Addition of macrophages to neural cultures further enhanced the toxic effect of HMGB1. To test whether immigrant macrophages in the ischemic brain mediate the RAGE effect, we generated chimeric mice by transplanting RAGE-/- bone marrow to wild-type mice. RAGE defi ciency in bone marrow-derived cells signifi cantly reduced the infarct size. Thus, HMGB1-RAGE signaling links necrosis with macrophage activation and may provide a target for anti-infl ammatory therapy in stroke.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.