Helveticoside was a biologically active component of seeds extract of Descurainia Sophia.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE65413 | GEO | 2015/01/30
SECONDARY ACCESSION(S): PRJNA273924
REPOSITORIES: GEO
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Project description:Apple seeds were subjected to accelerated aging. After 7, 14, and 21 days of aging, embryos were isolated. Part of the embryos were shortly fumigated with nitric oxide (NO). After 48 h of embryos culture (aged embryos or aged embryos treated with NO), embryonic axes were used to extract the total RNA. RT-qPCR were done to analyze the changes in the expression of genes related to seed aging. Short-term (3 h) treatment of embryos isolated from accelerated aged apple seeds (Malus domestica Borkh.) with NO partially reduced the effects of aging. The aim of the study was to investigate the impact of the short-term NO treatment of embryos isolated from apple seeds subjected to accelerated aging on the expression of genes potentially linked to the regulation of seed aging. Apple seeds were artificially aged for 7, 14, or 21 days. Then the embryos were isolated from the seeds, treated with NO, and cultured for 48 h. Progression of seeds aging was associated with the decreased transcript levels of most of the analyzed genes (Lea1, Lea2a, Lea4, Hsp70b, Hsp20a, Hsp20b, ClpB1, ClpB4, Cpn60a, Cpn60b, Raptor, and Saur). The role of NO in the mitigation of seed aging depended on the duration of the aging. After 7 and 14 days of seed aging, a decreased expression of genes potentially associated with the promotion of aging (Tor, Raptor, Saur) was noted. NO-dependent regulation of seed aging was associated with the stimulation of the expression of genes encoding chaperones and proteins involved in the repair of damaged proteins. After NO application, the greatest upregulation of ClpB, Pimt was noted in the embryos isolated from seeds subjected to 7-day long accelerated aging, Hsp70b, Hsp70c, Cpn in the embryos of seeds aged for 14 days, and Lea2a in the embryos of seeds after 21 days of aging.
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Project description:Experimental evidence in animal models suggests that misfolded Amyloid-? (A?) spreads in disease following a prion-like mechanism. Several properties characteristics of infectious prions have been shown for the induction of A? aggregates. However, a detailed titration of A? misfolding transmissibility and estimation of the minimum concentration of biologically active A? seeds able to accelerate pathological changes has not yet been performed. In this study, brain extracts from old tg2576 animals were serially diluted and intra-cerebrally injected into young subjects from the same transgenic line. Animals were sacrificed several months after treatment and brain slices were analyzed for amyloid pathology. We observed that administration of misfolded A? was able to significantly accelerate amyloid deposition in young mice, even when the original sample was diluted a million times. The titration curve obtained in this experiment was compared to the natural A? load spontaneously accumulated by these mice overtime. Our findings suggest that administration of the largest dose of A? seeds led to an acceleration of pathology equivalent to over a year. These results show that active A? seeds present in the brain can seed amyloidosis in a titratable manner, similarly as observed for infectious prions.
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