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.
Highlights
MethodsTraumatic brain injury (TBI) is an important contributor to worldwide mortality and morbidity, especially in young people, and is closely associated with decreased life expectancy[1]
The results show that Hydroxysafflor yellow A (HSYA) treatment can improve the function outcome of blood-brain barrier (BBB) after CCI injury
The effect of HSYA on the function of tight junctional proteins (TJPs) involved in BBB permeability following traumatic brain injury (TBI) injury 24 h was investigated by western blot and real-time polymerase chain reaction (PCR)
Summary
Traumatic brain injury (TBI) is an important contributor to worldwide mortality and morbidity, especially in young people, and is closely associated with decreased life expectancy[1]. It is a crucial medical, public health and socioeconomic problem around the world[1]. Pathophysiology of TBI involves two general stages: primary and secondary brain injury. After TBI, oxidative stress is generated and antioxidant enzymes decrease, resulting in neural dysfunction and cell death[2]. Recent observations showed that inflammation is closely related to the etiology and pathogenic mechanism of TBI, which is a crucial contributor to second brain damage. Toll-like receptor 4 (TLR4) could accelerate the secretion of various proinflammatory factors (IL-1, IL-6 and TNF-α) after combined with high-mobility group box-1 (HMGB1) and could rise enhanced secretion and release of proinflammatory cytokines via up-regulation of nuclear factor kappa-B (NF-κB)[3]
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