Attenuation of kirenol inflammationinduced by ischemic/reperfusion cerebral infarction stroke via TLR4/ NLRP3 signaling pathway: An in vivo approach

被引:0
|
作者
Yun, Debo [1 ]
Yang, Yujiao [2 ]
Shang, Bin [1 ]
Dong, Heng [1 ]
Luo, Bo [1 ]
Alahmadi, TahaniAwad [3 ,4 ]
Luo, Qing [5 ]
机构
[1] North Sichuan Med Coll, Nanchong Cent Hosp, Clin Med Coll 2, Dept Neurosurg, Nanchong City 637000, Peoples R China
[2] North Sichuan Med Coll, Affiliated Hosp, Dept Anesthesiol, Nanchong City 637000, Peoples R China
[3] King Saud Univ, Coll Med, Dept Pediat, Riyadh 11461, Saudi Arabia
[4] King Saud Univ, King Khalid Univ Hosp, Riyadh 11461, Saudi Arabia
[5] North Sichuan Med Coll, Nanchong Cent Hosp, Clin Med Coll 2, Dept Ultrasound, Nanchong City 637000, Peoples R China
关键词
Antioxidants; inflammation; inflammatory cytokines; ischemia-reperfusion stroke; kirenol; TLR4; NLRP3; ISCHEMIA-REPERFUSION INJURY; INFLAMMASOME; NEUROGENESIS; POLARIZATION;
D O I
10.4103/pm.pm_261_20
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Background: Ischemia/reperfusion (I/R)-induced stroke is a long-lasting disability. Numerous reports have demonstrated that inflammation is the major cause of ischemic cerebral injury. Therefore, it is important to develop an effective anti-inflammatory agent for the attenuation of I/R-induced brain injury. Objective: In this study, we examined the therapeutic role of kirenol against I/R-induced neuronal damage by inhibiting inflammation in Sprague-Dawley (SD) rats. Materials and Methods: I/R was induced in SD rats and subsequently were administered with 10 and 20 mg/kg of kirenol. Then, we assessed the neurological score, brain water content, and infarct size. The level of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione, and acetylcholinesterase, as well as the levels of malondialdehyde, was measured by using standard methods. The level of tumor necrosis factor (TNF)-alpha; interleukin (IL)-1 beta, IL-4, IL-6, and IL-10; and vascular endothelial growth factor was measured using standard kits. The targeted messenger RNA expression (NLRP3, NLRP4, TLR-4, TNF-alpha, caspase-1, ASC, and IL-1 beta) was quantified by polymerase chain reaction technique. Histopathological analysis of the brain tissue was performed. Results: According to our results, kirenol decreased the neurological deficit score, ameliorated the motor function, suppressed oxidative stress, reduced inflammation, and mediated the inhibition of TLR4/NLRP3-mediated inflammatory pathway. Conclusion: In conclusion, these findings demonstrate the protective effects of kirenol against I/R-induced cerebral injury. The mechanism of action is associated with the inhibition of inflammation through halting the TLR4/NLRP3 signaling pathway. In summary, kirenol is a potentially new compound which can be used to improve therapeutic strategies for stroke treatments.
引用
收藏
页码:268 / 274
页数:7
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