{'fraction_non_alphanumeric': 0.04092920353982301, 'fraction_numerical': 0.015486725663716814, 'mean_word_length': 4.835483870967742, '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}}
[Neuroprotective mechanism of hydrogen sulfide after cerebral ischemia-reperfusion in rats].

OBJECTIVE
To explore the neuroprotective mechanism of exogenous hydrogen sulfide after cerebral ischemia-reperfusion (I/R) in rats.


METHODS
A total of 240 male Sprague-Dawley rats were randomly divided into 4 groups of sham-operation group (I), I/R model group (II), low-dose sodium hydrosulfide (NaHS) group (III) and high-dose NaHS group (IV) (n = 60 each). Reversible middle cerebral artery occlusion (MCAO) model was established by intraluminal suture. However, the rats of group I were operated without a blockage of middle cerebral artery. The occlusions in other groups were removed after 2 h. And at 20 min pre-removal, normal saline, 50 µmol/kg NaHS, and 100 µmol/kg NaHS were injected into the abdomens of rats in groups II, III and IV respectively. At 6 h, 24 h, 48 h and 7 d post-reperfusion, behavioral test was performed to evaluate the neurological deficiency. And triphenyltetrazolium chloride (TTC) staining was used to observe the volume of cerebral infarction. In addition, the protein expressions of tumor necrosis factor-alpha (TNF-α) and heat shock protein 20 (HSP20) in ischemic cortex were measured by immunohistochemistry and Western blot.


RESULTS
Compared with I/R group, the neurological deficiency scores and volume of cerebral infarction of groups III and IV significantly decreased. Furthermore, the protein expression of HSP20 was markedly up-regulated in the groups III and IV while there was a marked down-regulation of TNF-α after reperfusion.


CONCLUSION
NaHS may exert anti-necrotic and anti-inflammatory function by inducing the expression of HSP20, inhibiting the expression of TNF-α and reducing the size of cerebral infarction so as to protect neurons after I/R injury.