Department of Plastic and Reconstructive Surgery, Faculty of Medical Faculty, Suleyman Demirel University, Isparta, Turkey.
Department of Biophysics, Faculty of Medical Faculty, Suleyman Demirel University, Isparta, Turkey.
J Pharm Pharmacol. 2019 Jan;71(1):83-92. doi: 10.1111/jphp.12741. Epub 2017 May 16.
This study was conducted to explore whether Hypericum perforatum L. (HPL) as a potent antioxidant protects against oxidative stress, cytokine production and caspase expression in muscle (soleus), brain and blood of sciatic nerve injury (SNI)-induced rats.
Thirty-five rats were equally divided into five groups. The first and second were used as untreated control and sham control groups, respectively. The third, fourth and fifth were sham + HPL, SNI and SNI + HPL groups, respectively. The third and fifth groups received 30 mg/kg HPL via gastric gavage for 28 days.
High levels of muscle, brain and red blood cell (RBC) lipid peroxidation, plasma cytokine (TNF-α, IL-1β and IL-2), muscle PARP, caspase 3 and 9 expression levels were decreased by HPL treatments. Plasma glutathione peroxidase (GPx) activity, α-tocopherol and melatonin, muscle, brain and RBC reduced glutathione (GSH) concentrations were decreased by SNI induction, whereas their values were increased by HPL treatments. β-carotene and retinol concentrations did not change in the five groups.
HPL may play a role in preventing SNI-induced inflammatory, oxidative and apoptotic blood, muscle and brain damages through upregulation of the GSH and GPx values but downregulation of PARP, caspase level and cytokine production in SNI-induced rats.
本研究旨在探讨贯叶连翘(HPL)作为一种有效的抗氧化剂,是否能防止坐骨神经损伤(SNI)诱导的大鼠肌肉(比目鱼肌)、大脑和血液中的氧化应激、细胞因子产生和半胱天冬酶表达。
35 只大鼠被平均分为 5 组。第一组和第二组分别作为未处理对照组和假手术对照组。第三组、第四组和第五组分别为假手术+ HPL、SNI 和 SNI+HPL 组。第三组和第五组通过灌胃给予 30mg/kg HPL,共 28 天。
HPL 处理降低了肌肉、大脑和红细胞(RBC)的脂质过氧化水平、血浆细胞因子(TNF-α、IL-1β 和 IL-2)、肌肉 PARP、半胱天冬酶 3 和 9 的表达水平。SNI 诱导降低了血浆谷胱甘肽过氧化物酶(GPx)活性、α-生育酚和褪黑素、肌肉、大脑和 RBC 中的还原型谷胱甘肽(GSH)浓度,而 HPL 处理则增加了这些值。5 组β-胡萝卜素和视黄醇浓度没有变化。
HPL 可能通过上调 GSH 和 GPx 值,下调 PARP、半胱天冬酶水平和细胞因子产生,在 SNI 诱导的大鼠中发挥作用,防止 SNI 诱导的血液、肌肉和大脑的炎症、氧化和凋亡损伤。