Aydogmus Evren, Gul Sanser, Bahadir Burak
Department of Neurosurgery, University of Health Sciences, Dr. Lutfi Kirdar Kartal Training and Research Hospital, Istanbul, Turkey.
Department of Neurosurgery, Bulent Ecevit University Hospital, Zonguldak, Turkey.
World Neurosurg. 2019 Feb;122:e1332-e1337. doi: 10.1016/j.wneu.2018.11.043. Epub 2018 Nov 15.
We examined the protective effects of hesperidin on cerebral vasospasm by establishing an experimental rat model of subarachnoid hemorrhage and performing biochemical, pathologic, and histomorphometric analysis on these data.
Forty albino Wistar rats were randomly divided into 5 groups of n = 8 in each: group (G)1, no experimental interventions; G2, subjected to subarachnoid hemorrhage; G3, subjected to subarachnoid hemorrhage and administered saline (100 mg/kg); G4, subjected to subarachnoid hemorrhage and treated with low-dose hesperidin (50 mg/kg); and G5, subjected to subarachnoid hemorrhage and treated with high-dose hesperidin (100 mg/kg). Subarachnoid hemorrhage was created by injecting 0.15 cc of autologous blood taken from the rat-tail artery and injected into the cisterna magna from the craniocervical junction. Drugs were administered intraperitoneally as twice daily doses for 48 hours. Rats were euthanized at the end of this period.
No statistically significant decrease was observed in malondialdehyde levels, which is the end-product of lipid peroxidation, among the drug groups (G4 and G5). Thin sections prepared from the basilar artery were examined morphologically. Severe luminal narrowing and vessel-wall thickening were observed in the subarachnoid hemorrhage groups (G2, G3). In the hesperidin-administered groups (G4, G5), it was determined that vessel wall thickness measurements revealed thinner walls than in the subarachnoid hemorrhage groups (G2, G3) and the luminal diameters were significantly larger than in the subarachnoid hemorrhage groups (G2, G3).
These findings suggest that hesperidin has no effect on malondialdehyde-associated lipid-peroxidation activity; however, it might be useful in subarachnoid hemorrhage therapy because of its beneficial effects on vessel wall thickness and luminal diameters.
通过建立大鼠蛛网膜下腔出血实验模型,并对这些数据进行生化、病理和组织形态计量学分析,研究橙皮苷对脑血管痉挛的保护作用。
将40只白化Wistar大鼠随机分为5组,每组n = 8:第1组(G1),无实验干预;G2组,进行蛛网膜下腔出血;G3组,进行蛛网膜下腔出血并给予生理盐水(100 mg/kg);G4组,进行蛛网膜下腔出血并给予低剂量橙皮苷(50 mg/kg);G5组,进行蛛网膜下腔出血并给予高剂量橙皮苷(100 mg/kg)。通过从大鼠尾动脉采集0.15 cc自体血并从颅颈交界处注入枕大池来制造蛛网膜下腔出血。药物以每日两次的剂量腹腔注射,持续48小时。在此期间结束时对大鼠实施安乐死。
在药物组(G4和G5)中,未观察到脂质过氧化终产物丙二醛水平有统计学意义的降低。对基底动脉制备的薄片进行形态学检查。在蛛网膜下腔出血组(G2、G3)中观察到严重的管腔狭窄和血管壁增厚。在给予橙皮苷的组(G4、G5)中,确定血管壁厚度测量显示其壁比蛛网膜下腔出血组(G2、G3)更薄,管腔直径明显大于蛛网膜下腔出血组(G2、G3)。
这些发现表明橙皮苷对丙二醛相关的脂质过氧化活性没有影响;然而,由于其对血管壁厚度和管腔直径的有益作用,它可能对蛛网膜下腔出血治疗有用。