{'fraction_non_alphanumeric': 0.025934861278648975, 'fraction_numerical': 0.009650180940892641, 'mean_word_length': 5.260377358490566, '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}}
The gender difference in effect of sevoflurane exposure on cognitive function and hippocampus neuronal apoptosis in rats.

OBJECTIVE
Anesthesia and surgery can induce postoperative cognitive dysfunction. Ser-133 phosphorylation sites of cAMP-response element binding protein (CREB) is a key gene that mediate a variety of downstream transcription initiation factors, regulate neuronal survival and promote the expression of a large number of genes. Thus, CREB may play a role in this impairment. We hypothesize that and sevoflurane-induced cognitive impairment possibly via inhibiting the expression of CREB downstream genes and proteins.


MATERIALS AND METHODS
To test this hypothesis, adult Sprague-Dawley rats were subjected to sevoflurane exposure and were tested with a series of behavioral experiments (open field, passive avoidance test and Morris water maze test) at different time (1 d to 95 d). Besides, blood gas changes and expiratory sevoflurane concentrations were examined at 2 h; the levels of phosphorylated CREB 1, the protein Bcl-2, Caspase-8 and Caspase-3 were assessed at 1 week and 3 months after anesthesia. We also conducted a comparison in sevoflurane-induced cognitive impairment between male and female rats.


RESULTS AND CONCLUSIONS
Here, we found that sevoflurane anesthesia can impair short-term cognitive function, which may be via down-regulating p-CREB1 and Bcl-2 expression and up-regulating Caspase-8 expression to reduce hippocampus neuronal apoptosis, and male rats suffered a more severe cognitive dysfunction than female rats. In addition, sevoflurane can produce a reversible long-term cognitive dysfunction in rats.