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作 者:翟凤国[1] 李厚忠[1] 周福波[1] 林峰[1] 关利新[1]
机构地区:[1]牡丹江医学院药理学教研室,黑龙江牡丹江157011
出 处:《医学综述》2015年第24期4539-4540,4546,共3页Medical Recapitulate
基 金:黑龙江省自然科学基金(H201379);黑龙江省教育厅科学技术研究项目(11551527);黑龙江省卫生厅科研课题(2012-276)
摘 要:目的探讨蒺藜皂苷对局灶性脑缺血大鼠脑组织过氧化物酶体增殖物激活受体γ(PPARγ)和核因子κB(NF-κB)炎症信号途径表达的影响,并进一步探讨其潜在的机制。方法将40只SD大鼠依据随机数字表法分为假手术组、模型组和蒺藜皂苷低剂量组和高剂量组,每组10只,采用线栓法制备大鼠脑缺血/再灌注损伤模型。脑缺血/再灌注24 h后检测大鼠神经功能损伤评分;酶联免疫吸附测定法检测大鼠脑组织NF-κB、肿瘤坏死因子α(TNF-α)和白细胞介素(IL)1β的水平;免疫印迹法检测大鼠脑组织PPARγ蛋白表达水平。结果与模型组比较,蒺藜皂苷治疗低剂量组和高剂量组大鼠神经功能损伤明显减轻[(1.8±0.7)分、(1.3±0.5)分比(2.3±0.7)分],差异有统计学意义(P<0.05);与模型组NF-κB、TNF-α、IL-1β[(18.4±1.5)μg/mg、(916±128)pg/mg、(169±16)pg/mg]比较,蒺藜皂苷低剂量[(16.4±1.3)μg/mg、(257±110)pg/mg、(148±16)pg/mg]和高剂量组[(15.0±1.2)μg/mg、(665±72)pg/mg、(139±14)pg/mg]缺血脑组织NF-κB、TNF-α和IL-1β水平明显降低(P<0.05)。结论蒺藜皂苷可能通过激活PPARγ的表达,进而抑制NF-κB炎症信号途径,抑制炎性因子的表达,降低炎症反应,从而减轻大鼠脑缺血/再灌注损伤而发挥其神经保护作用。Objective To study and explore the effect of tribulus terrestris on the expression of peroxisome proliferators γ( PPAR γ) and nuclear factor κB( NF-κB) inflammatory signaling pathways in rat brain tissue after focal cerebral ischemia,and further explore its potential mechanisms. Methods According to random number table method,40 SD rats were randomly equally divided into sham operation group,cerebral ischemia-reperfusion model group,low-dose saponins of tribulus terrestris group and high-dose saponins of tribulus terrestris group. Cerebral ischemia reperfusion model was established with suture emboli method in middle cerebral artery of rats. Neurological deficit scores was measured 24 hours after the cerebral reperfusion. Content of NF-κB,tumor necrosis factor-α( TNF-α) and interleukin-1β( IL-1β) in rat brain was detected by ELISA; expression levels of PPARγ protein in rat brain was determined by Western blot. Results Compared with the model group,nerve function injury of low dose tribulus terrestris saponin treatment group and high dose group obviously reduced[( 1. 8 ± 0. 7) scores,( 1. 3 ± 0. 5) scores vs( 2. 3 ± 0. 7) scores],the difference was statistically significant( P〈0. 05). NF-κB,TNF-α and IL-1 β level of low dose saponins of tribulus group [( 16. 4 ± 1. 3) μg / mg,( 257 ± 110) pg / mg,( 148 ± 16) pg / mg]and high dose group[( 15. 0 ± 1. 2) μg/mg,( 665 ± 72) pg/mg,( 139 ± 14) pg/mg]were lower than those of the model group[( 18. 4 ± 1. 5) μg/mg,( 916 ± 128) pg/mg,( 169 ± 16) pg/mg]( P〈0. 05). Conclusion Saponins of tribulus terrestris exerts the neuroprotective effect on cerebral ischemia-reperfusion injury in rats through inhibiting the inflammatory reaction,which may be associated with the increase of the PPARγ protein expression and inhibition of NF-κB inflammation signal pathway.
关 键 词:脑缺血/再灌注 蒺藜皂苷 炎症 核因子ΚB 过氧化物酶体增殖物激活受体Γ
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