کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6262947 1613817 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research ReportRifampicin attenuates rotenone-induced inflammation via suppressing NLRP3 inflammasome activation in microglia
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Research ReportRifampicin attenuates rotenone-induced inflammation via suppressing NLRP3 inflammasome activation in microglia
چکیده انگلیسی


- Rifampin inhibits gene expression and release of IL-1β in rotenone-treated microglia.
- Rifampicin regulates neuroinflammation via inhibiting NLRP3 inflammasome activation.
- Rifampicin reduces rotenone-induced ROS and loss of mitochondrial membrane potential.
- Rifampicin emerges as a promising candidate for modulating neuroinflammation in PD.

A growing body of evidence has supported that environmental factors, such as exposure to heavy metal and pesticides, play an important role in the pathogenesis of Parkinson׳s disease (PD). Rotenone, the active ingredient in various pesticides, has been identified as an inducer of PD. It has been revealed that rotenone induces activation of microglia and generation of pro-inflammatory factors in PD. Our previous studies demonstrated that rifampicin possessed neural protective effect in PD. In this study, we aimed to study the effect of rifampicin on the inflammation induced by rotenone in microglia and the underlying mechanisms. Results demonstrated that rifampicin pretreatment significantly reduced rotenone-induced cytotoxicity and gene expression of IL-1β in BV2 microglia. Moreover, western blot analysis verified that rifampicin pretreatment suppressed NLRP3 inflammasome activation via inhibiting caspase-1 cleavage and protein expression of NLRP3. As it is indicated that reactive oxidative stress (ROS) is one of the activators for NLRP3 inflammasome, we further employed 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) staining and Rhodamine123 staining to detect intracellular ROS and mitochondrial membrane potential (MMP), respectively. Results confirmed that rifampicin obviously reduced intracellular ROS and reversed loss of MMP in BV2 cells treated by rotenone. Taken together, our data indicate that rifampicin pretreatment inhibits maturation of IL-1β and neuroinflammation induced by rotenone via attenuating NLRP3 inflammasome activation. Rifampicin might emerge as a promising candidate for modulating neuroinflammation in PD.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1622, 5 October 2015, Pages 43-50
نویسندگان
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