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Hydroxysafflor yellow A acutely attenuates blood-brain barrier permeability, oxidative stress, inflammation and apoptosis in traumatic brain injury in rats1
Xu, Jianjun; Zhan, Tian; Zheng, Wan; Huang, Yun-Ke; Chen, Ken; Zhang, Xian-Hua; Ren, Ping; Huang, Xi.
  • Xu, Jianjun; Nanjing University of Chinese Medicine. CN
  • Zhan, Tian; Nanjing University of Chinese Medicine. Department of TCM-related comorbid depression. CN
  • Zheng, Wan; Nanjing University of Chinese Medicine. CN
  • Huang, Yun-Ke; Womens Hospital School of Medicine Zhejiang University. CN
  • Chen, Ken; Nanjing University of Chinese Medicine. Department of TCM-related comorbid depression. CN
  • Zhang, Xian-Hua; Xiamen Xianyue Hospital. Xiamen Mental Health Center. CN
  • Ren, Ping; Affiliated hospital Nanjing University of Chinses Medicine. Department of Geriatrics. CN
  • Huang, Xi; Nanjing University of Chinese Medicine. Department of TCM-related comorbid depression. CN
Acta cir. bras ; 35(12): e351202, 2020. tab, graf
Article in English | LILACS | ID: biblio-1152683
ABSTRACT
Abstract

Purpose:

To investigate the therapeutic benefits of Hydroxysafflor yellow A (HSYA) on blood-brain barrier (BBB) vulnerability after traumatic brain injury (TBI) and identify its potential action of mechanisms on TBIinduced injuries.

Methods:

The rat TBI model was performed by using a controlled cortical impact device. The BBB permeability induced by TBI was measured through Evans Blue dye superflux and western blotting or polymerase chain reaction (PCR) for tight junctional proteins (TJPs). The post-TBI changes in oxidative stress markers, inflammatory response and neuron apoptosis in brain tissue were also tested.

Results:

Herein, the results showed that HSYA acutely attenuated BBB permeability via increasing the production of the TJPs, including occludin, claudin-1 and zonula occludens protein 24 h after TBI. Additionally, HSYA could suppress the secretion of proinflammatory factors, such as interleukin-1β, interleukin-6, and tumor necrosis factor-α (IL-1β, IL-6, and TNF-α), and also concurrently down-regulate the expression of inflammation-related Toll-like receptor 4/nuclear factor kappa-B (TLR4/NF-kB) protein. These HSYA challenged changes were accompanied by the decreased TBI induced oxidative stress markers and inhibited the expression of apoptosis proteins Bax, caspase-3 and caspase-9.

Conclusions:

Taken together, all findings suggested that HSYA (30 mg/kg) are against TBI through improving the integrity in BBB, which are associated with the antioxidant, anti-inflammation and antiapoptosis via the probable mechanism of down-regulation of the TLR4/NF-kB pathway, and its in-detail protective mechanisms are under study.
Subject(s)


Full text: Available Index: LILACS (Americas) Main subject: Blood-Brain Barrier / Brain Injuries, Traumatic Type of study: Prognostic study Limits: Animals Language: English Journal: Acta cir. bras Journal subject: General Surgery / Procedimentos Cir£rgicos Operat¢rios Year: 2020 Type: Article Affiliation country: China Institution/Affiliation country: Affiliated hospital Nanjing University of Chinses Medicine/CN / Nanjing University of Chinese Medicine/CN / Womens Hospital School of Medicine Zhejiang University/CN / Xiamen Xianyue Hospital/CN

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Full text: Available Index: LILACS (Americas) Main subject: Blood-Brain Barrier / Brain Injuries, Traumatic Type of study: Prognostic study Limits: Animals Language: English Journal: Acta cir. bras Journal subject: General Surgery / Procedimentos Cir£rgicos Operat¢rios Year: 2020 Type: Article Affiliation country: China Institution/Affiliation country: Affiliated hospital Nanjing University of Chinses Medicine/CN / Nanjing University of Chinese Medicine/CN / Womens Hospital School of Medicine Zhejiang University/CN / Xiamen Xianyue Hospital/CN