RESUMO
Proline has been reported to play an important role in helping plants cope with several stresses, including salinity. This study investigates the relationship between proline accumulation and salt tolerance in an accession of Australian wild rice Oryza australiensis Domin using morphological, physiological, and molecular assessments. Seedlings of O. australiensis wild rice accession JC 2304 and two other cultivated rice Oryza sativa L. cultivars, Nipponbare (salt-sensitive), and Pokkali (salt-tolerant), were screened at 150 mM NaCl for 14 days. The results showed that O. australiensis was able to rapidly accumulate free proline and lower osmotic potential at a very early stage of salt stress compared to cultivated rice. The qRT-PCR result revealed that O. australiensis wild rice JC 2304 activated proline synthesis genes OsP5CS1, OsP5CS2, and OsP5CR and depressed the expression of proline degradation gene OsProDH as early as 1 h after exposure to salinity stress. Wild rice O. australiensis and Pokkali maintained their relative water content and cell membrane integrity during exposure to salinity stress, while the salt-sensitive Nipponbare failed to do so. An analysis of the sodium and potassium contents suggested that O. australiensis wild rice JC 2304 adapted to ionic stress caused by salinity by maintaining a low Na+ content and low Na+/K+ ratio in the shoots and roots. This demonstrates that O. australiensis wild rice may use a rapid accumulation of free proline as a strategy to cope with salinity stress.
RESUMO
Our previous studies reported that methanol extract of Sanguisorbae radix from Sanguisorba officinalis L. (Rosaceae) prevented neuronal cell damage induced by Abeta (25-35) in vitro. The present study was carried out to investigate the effect of gallic acid isolated from Sanguisorbae radix on Abeta (25-35)-induced neurotoxicity using cultured rat cortical neurons. Gallic acid (0.1, 1 microM) showed a concentration-dependent inhibition on Abeta (25-35) (10 microM)-induced apoptotic neuronal death, as assessed by a 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33,342 staining. Pretreatment of gallic acid inhibited 10 microM Abeta (25-35)-induced elevation of cytosolic Ca(2+) concentration ([Ca(2+)](c)) and generation of reactive oxygen species (ROS), which were measured by fluorescent dyes. Gallic acid also inhibited glutamate release into medium induced by 10 microM Abeta (25-35), which was measured by HPLC. These results suggest that gallic acid prevents Abeta (25-35)-induced apoptotic neuronal death by interfering with the increase of [Ca(2+)](c), and then by inhibiting glutamate release and generation of ROS, and that these effects of gallic acid may be partly associated with the neuroprotective effect of Sanguisorbae radix.
