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½üÆÚ¡¶Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition¡·ÔÚ Acta Biochimica et Biophysica Sinica£¨ÉúÎﻯѧÓëÉúÎïÎïÀíѧ±¨£©½ÒÏþ ¡£¸ÃÑо¿ÓÉÎ÷ºþ´óѧҽѧԺÁ¥Êôº¼ÖÝÊеÚÒ»ÈËÃñÒ½ÔºÉñ¾Íâ¿ÆºÍÌå¼ìÖÐÐÄÍŶÓÍê³É ¡£¸ÃÑо¿Åú×¢ £¬Ê¯É¼¼î¼××¢ÉäÒº¿ÉÒÖÖÆÄÚƤϸ°û½¹Íö¡¢¿¹Ñõ»¯Ó¦¼¤ £¬¸ÄÉÆÖëÍøĤÏÂÇ»³öѪ£¨SAH£©ºóµÄÔçÆÚÄÔËðÉË ¡£
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Subarachnoid hemorrhage (SAH) is a severe stroke type [1,2] mainly caused by aneurysm rupture and is characterized by high morbidity and mortality [3]. Additionally, survivors often have cognitive impairments affecting patients’ daily functionality, labor capacity, and quality of life [4]. Early brain injury within 72 h is considered to be the main cause of poor prognosis in SAH patients [5]. Alleviating early brain damage contributes to the improvement on survival rate and prognosis of SAH patients [6,7]. Therefore, inhibiting early brain damage in SAH patients is an important therapeutic strategy for improving the prognosis of SAH patients. It has been revealed that neuronal apoptosis and blood-brain barrier (BBB) destruction are the hallmark events of early brain injury after SAH, are closely related to irreversible acute brain injury after SAH, and are important factors for poor prognosis in SAH patients [8,9]. In addition, the increased permeability of the BBB allows immune molecules to migrate to the brain parenchyma, which further exacerbates brain injury. It is suggested that inhibiting BBB dysfunction can effectively ameliorate early brain injury after SAH and is an important therapeutic method for improving the prognosis of SAH patients.
ÖëÍøĤÏÂÇ»³öѪ£¨SAH£©ÊÇÒ»ÖÖÑÏÖصÄÄÔ×äÖÐÀàÐÍ[1,2] £¬Ö÷ÒªÓÉÂÄÚ¶¯ÂöÁöÆÆËéÒýÆ𠣬ÆäÌصãÊǸßÖ²ÐÂʺ͸ßéæÃüÂÊ[3] ¡£±ðµÄ £¬ÐÒ´æÕßͨ³£±£´æÈÏÖªÕÏ° £¬Ó°Ï컼ÕßµÄÒ»Ñùƽ³£¹¦Ð§¡¢ÀͶ¯ÄÜÁ¦ºÍÉúÑÄÖÊÁ¿[4] ¡£SAHºó72 СʱÄÚµÄÔçÆÚÄÔËðÉ˱»ÒÔΪÊÇÓ°ÏìSAH »¼ÕßÔ¤ºó²»Á¼µÄÖ÷ÒªÔµ¹ÊÔÓÉÖ®Ò»[5] ¡£¼õÇáÔçÆÚÄÔËðÉËÓÐÖúÓÚ¸ÄÉÆ SAH »¼ÕßµÄÉúÑÄÂʺÍÔ¤ºó[6,7] ¡£Òò´Ë £¬ÒÖÖÆ SAH »¼ÕßÔçÆÚÄÔËðÉËÊǸÄÉÆ SAH »¼ÕßÔ¤ºóµÄÖ÷ÒªÖÎÁÆÕ½ÂÔ ¡£Ñо¿Åú×¢ £¬Éñ¾ÔªµòÍöºÍѪÄÔÆÁÕÏ£¨BBB£©ÆÆËðÊÇ SAHºóÔçÆÚÄÔËðÉ˵ıê¼ÇÐÔÊÂÎñ £¬Óë SAHºó²»¿ÉÄæµÄ¼±ÐÔÄÔËðÉËÇ×½üÏà¹Ø £¬ÊÇ SAH »¼ÕßÔ¤ºó²»Á¼µÄÖ÷ÒªÒòËØ[8,9] ¡£±ðµÄ £¬ÑªÄÔÆÁÕϵÄͨ͸ÐÔÔöÌíʹÃâÒß·Ö×ÓǨáãµ½ÄÔʵÖÊ £¬Õâ½øÒ»²½¼Ó¾çÁËÄÔËðÉË ¡£Ñо¿Åú×¢ £¬ÒÖÖÆѪÄÔÆÁÕϹ¦Ð§ÕÏ°¿ÉÓÐÓøÄÉÆ SAHºóµÄÔçÆÚÄÔËðÉË £¬ÊǸÄÉÆ SAH »¼ÕßÔ¤ºóµÄÖ÷ÒªÒªÁì ¡£
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Animal handling
SPF male SD rats were fed according to standard animal care proposal. After one week of adaptive feeding, the following treatments were carried out: (1) sham group: SD rats were subjected to a sham operation; (2) model group: SD rats were treated for SAH, and saline was applied intraperitoneally; and (3) treatment group: SD rats were treated for SAH, and Huperzine A (0.1 mg/kg, WEPON, Drug Approval Number: H20183340) was applied intraperitoneally. The procedure was as follows: after the SD rats were anesthetized, 0.35 mL of fresh autologous blood (20 s) without heparin was slowly injected into the anterior cistern of the optic chiasm, and the animals were kept head down at 30¡æ for 20 min. The rats were immediately injected with 2 mL of normal saline and returned to the cage alone. The body temperature was maintained at 37°C. In the sham group, the SD rats (male, 250 -300 g) were injected with normal saline instead of autologous blood; in the model group and treatment group, the placebo (saline) and Huperzine A were administered intraperitoneally 12 h after autologous blood injection.
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