Ganoderic acid A protects neural cells against NO stress injury in vitro via stimulating β adrenergic receptors

• 来源期刊: 中国药理学报（英文版）
• 关键词: β-adrenergic receptors sodium nitroprusside (SNP) SH-SY5Y cells PC12 cells ganoderic acid A adrenaline norepinephrine phentolamine metoprolol ICI 118551
• 年，卷（期）: 2020,（4）
• 页码范围: 516-522
• 页数: 7页
• 语种: 英文

摘要

Excessive nitric oxide (NO) causes extensive damage to the nervous system,and the adrenergic system is disordered in many neuropsychiatric diseases.However,the role of the adrenergic system in protection of the nervous system against sodium nitroprusside (SNP) injury remains unclear.In this study,we investigated the effect of ganoderic acid A (GA A) against SNP injury in neural cells and the role of adrenergic receptors in GA A neuroprotection.We found that SNP (0.125-2 mM) dosedependently decreased the viability of both SH-SYSY and PC12 cells and markedly increased NO contents.Pretreatment with GA A (10 μM) significantly attenuated SNP-induced cytotoxicity and NO increase in SH-SY5Y cells,but not in PC12 cells.Furthermore,pretreatment with GA A caused significantly higher adrenaline content in SH-SYSY cells than in PC12 cells.In order to elucidate the mechanism of GA A-protecting SH-SYSY cells,we added adrenaline,phentolamine,metoprolol,or ICI 118551 1 h before GA A was added to the culture medium.We found that addition of adrenaline (10 μM) significantly improved GA A protection in PC12 cells.The addition of β1-adrenergic receptor antagonist metoprolol (10 μM) or β2-adrenergic receptor antagonist ICI 118551 (0.1 μM) blocked the protective effect of GA A,whereas the addition of α-adrenergic receptor antagonist phentolamine (0.1 μM) did not affect GA A protection in SH-SYSY cells.These results suggest that β-adrenergic receptors play an important role in the protection of GA A in SH-SYSY cells against SNP injuries,and excessive adrenaline system activation caused great damage to the nervous system.