Satureja khuzistanica Jamzad essential oil and pure carvacrol attenuate TBI-induced inflammation and apoptosis via NF-κB and caspase-3 regulation in the male rat brain.
Satureja khuzistanica Jamzad essential oil and pure carvacrol attenuate TBI-induced inflammation and apoptosis via NF-κB and caspase-3 regulation in the male rat brain.
复制标题
DOI：
10.1038/s41598-023-31891-3
复制
发表时间：
2023-03-23
影响因子：
4.6
通讯作者：
Thomas, Theresa Currier
中科院分区：
文献类型：
--
作者：
Abbasloo, Elham;Amiresmaili, Sedigheh;Shirazpour, Sara;Khaksari, Mohammad;Kobeissy, Firas;Thomas, Theresa Currier
创伤性脑损伤（TBI）引起进行性功能障碍，诱发生化和代谢变化，导致细胞死亡。然而，目前还没有明确的fda批准的治疗TBI的方法。我们之前的免疫组化结果表明，具有成本效益的天然伊朗药物Satureja khuzistica Jamzad精油（SKEO）含有94.16%的carvacrol (CAR)，具有减少神经元死亡和炎症标志物、激活星形胶质细胞和改善神经系统预后等有益作用。然而，这些神经保护作用的分子机制尚未阐明。本研究探讨了TBI诱导后SKEO和CAR抗炎和抗凋亡的可能机制。84只雄性Wistar大鼠随机分为6组：Sham组、TBI组、TBI + Vehicle组、TBI + CAR组（100、200 mg/kg）和TBI + SKEO组（200 mg/kg）。建立“Marmarou”减重模型后，在大鼠脑内诱导弥漫性脑损伤。TBI诱导后30分钟，腹腔注射SKEO和CAR。脑外伤后1天，损伤大鼠表现出明显的脑水肿、神经行为障碍和神经元凋亡。Western blot结果显示，cleaved caspase-3、NFκB p65和Bax/Bcl-2比值上调，CAR和SKEO （200 mg/kg）可减弱这种上调。此外，ELISA结果显示，CAR治疗可显著阻止脑促炎细胞因子的过量产生，包括IL-1β、TNF-α和IL-6。此外，神经元特异性烯醇化酶（NSE）免疫组化结果显示，CAR和SKEO对脑损伤后神经元死亡具有保护作用。目前的研究表明，SKEO和CAR可能的神经保护机制可能与（至少部分）调节NF-κB调节的炎症和caspase-3蛋白表达有关。这也表明CAR对TBI的保护作用比SKEO更有效。然而，SKEO和CAR的使用可能是一种新的治疗方法，可以改善tbi相关的二期神经病理结果。
Traumatic brain injury (TBI) causes progressive dysfunction that induces biochemical and metabolic changes that lead to cell death. Nevertheless, there is no definitive FDA-approved therapy for TBI treatment. Our previous immunohistochemical results indicated that the cost-effective natural Iranian medicine, Satureja khuzistanica Jamzad essential oil (SKEO), which consists of 94.16% carvacrol (CAR), has beneficial effects such as reducing neuronal death and inflammatory markers, as well as activating astrocytes and improving neurological outcomes. However, the molecular mechanisms of these neuroprotective effects have not yet been elucidated. This study investigated the possible mechanisms involved in the anti-inflammatory and anti-apoptotic properties of SKEO and CAR after TBI induction. Eighty-four male Wistar rats were randomly divided into six groups: Sham, TBI, TBI + Vehicle, TBI + CAR (100 and 200 mg/kg), and TBI + SKEO (200 mg/kg) groups. After establishing the “Marmarou” weight drop model, diffuse TBI was induced in the rat brain. Thirty minutes after TBI induction, SKEO & CAR were intraperitoneally injected. One day after TBI, injured rats exhibited significant brain edema, neurobehavioral dysfunctions, and neuronal apoptosis. Western blot results revealed upregulation of the levels of cleaved caspase-3, NFκB p65, and Bax/Bcl-2 ratio, which was attenuated by CAR and SKEO (200 mg/kg). Furthermore, the ELISA results showed that CAR treatment markedly prevents the overproduction of the brain pro-inflammatory cytokines, including IL-1β, TNF-α, and IL-6. Moreover, the neuron-specific enolase (NSE) immunohistochemistry results revealed the protective effect of CAR and SKEO on post-TBI neuronal death. The current study revealed that the possible neuroprotective mechanisms of SKEO and CAR might be related to (at least in part) modulating NF-κB regulated inflammation and caspase-3 protein expression. It also suggested that CAR exerts more potent protective effects than SKEO against TBI. Nevertheless, the administration of SKEO and CAR may express a novel therapeutic approach to ameliorate TBI-related secondary phase neuropathological outcomes.
登录
查看更多内容
米托醌有助于对抗慢性时间点开放性头部创伤性脑损伤的神经、认知和分子后果。
影响因子：
4.7
作者：
Haidar MA;Shakkour Z;Barsa C;Tabet M;Mekhjian S;Darwish H;Goli M;Shear D;Pandya JD;Mechref Y;El Khoury R;Wang K;Kobeissy F
通讯作者：
Kobeissy F
DOI：
10.1016/0169-328x(96)00059-9
发表时间：
1996-09-01
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
Gillardon, F;Lenz, C;Kuschinsky, W
通讯作者：
Kuschinsky, W
影响因子：
2
作者：
Cernak, I;Chapman, SM;Vink, R
通讯作者：
Vink, R
影响因子：
6.9
作者：
Chodobski A;Zink BJ;Szmydynger-Chodobska J
通讯作者：
Szmydynger-Chodobska J
影响因子：
5.4
作者：
Freire, CMM;Marques, MOM;Costa, M
通讯作者：
Costa, M