{'fraction_non_alphanumeric': 0.03460514640638864, 'fraction_numerical': 0.0044365572315882874, 'mean_word_length': 5.301675977653631, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Protective effects of AST and ASI on memory impairment and its mechanism in senescent rats treated by GC].

OBJECTIVE
To study the protective effects and mechanisms of astragaloside (AST) and astragalus saponin I (ASI) on the memory impairment in senescent rats treated by glucocorticoid (GC).


METHOD
Y maze test was performed to determine the effects of AST and ASI on memory impairment of hydrocortisone(HC)-induced senescent rats. Using Ca2+ sensitive fluorescent indicator (Furo-2), free intracellular calcium concentration ([Ca2+]i) was measured by double wavelength fluorescence sepectrophotometer in thymocytes and hippocampal neurons induced dexamethasone (DEX). And apoptosis was detected by DNA gel electrophoresis and flow cytometry.


RESULT
Compared with HC control, AST and ASI can improve the memory of the senescent rats treated by HC, lower [Ca2+]i and suppress apoptosis of thymocytes and hippocampal neurons induced by DEX.


CONCLUSION
AST and ASI can delay the aging in rats treated by HC, and its mechanism may includ lowering[Ca2+]i and suppressing the apoptosis of thymocytes and hippocampal neurons.