Tetrahydroxy stilbene glucoside ameliorates H2O2-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
- Zhao Jiang
- Wenhong Wang
- Chengcheng Guo
Affiliations: Department of Neurology, Tianjin First Central Hospital, Tianjin 300192, P.R. China
- Published online on: August 10, 2017 https://doi.org/10.3892/mmr.2017.7225
Copyright: © Jiang
et al. This is an open access article distributed under the
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Commons Attribution License.
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Tetrahydroxy stilbene glucoside (TSG) is one of the main active ingredients of Polygonum multiflorum and performs various types of biological activity, particularly anti‑inflammatory and anti‑oxidative activities. However, the beneficial effect of TSG in H2O2‑induced human brain microvascular endothelial cell (HBMEC) dysfunction has not been fully elucidated. In the present study, H2O2‑induced oxidative stress and inflammatory responses, and the pharmacological effect of TSG were investigated. The results demonstrated that H2O2 appeared to exert a cytotoxic effect on HBMECs, as the cell viability was significantly inhibited in H2O2‑treated HBMECs. Conversely, TSG did not exert a toxic effect on HBMECs, and TSG inhibited H2O2‑induced HBMEC cytotoxicity in a dose‑dependent manner. Furthermore, the findings indicated that TSG restricted the oxidative stress caused by H2O2 via inhibition of malondialdehyde and reactive oxygen species, and upregulation of superoxide dismutase and glutathione. H2O2‑induced injury was associated with enhancing the levels of inflammatory cytokines, tumor necrosis factor‑α, interleukin (IL)‑6 and IL‑1β in the cultured HBMECs, which were attenuated by TSG treatment. Furthermore, the findings demonstrated that TSG inhibited necrosis factor‑κB protein expression levels, which, as an upstream transcription factor, may regulate inflammatory responses. Thus, TSG protected HBMECs from H2O2‑induced dysfunction by inhibiting oxidative stress and inflammatory responses.