Sodium tanshinone IIA sulfonate attenuates hemorrhagic shock-induced organ damages by nuclear factor-kappa B pathway.

BACKGROUND: Trauma resulted hemorrhagic shock (HS) leads to increased oxidative stress and inflammatory responses, which contributes greatly to organ failure or dysfunction. Tanshinone IIA sulfonate (TSA), as an antioxidant, may potentially be used in fluid resuscitation to prevent HS-induced organ damages.

METHODS: In this study, a rat HS model was constructed. HS rats received TSA or vehicle drug during resuscitation. Mean arterial pressure and factors associated with organ failure or dysfunction, oxidative stress, and inflammatory response were investigated to evaluate treatment responses. Expression of proteins in NF-кB pathway was evaluated to elucidate the mechanism of TSA in preventing HS-induced organ damage.

RESULTS: Although HS induced organ damage and upregulated oxidative stress and inflammatory response, TSA treatment ameliorated organ dysfunction, reduced oxidative stress, and suppressed inflammatory responses. We also showed that TSA treatment attenuated HS-induced activation in NF-кB pathway.

CONCLUSIONS: TSA can potentially serve as an antioxidant for ameliorating HS-induced organ failure or function. Its mechanism of action may be through inhibiting NF-кB pathway.