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. 2016 Oct;14(4):3690-6.
doi: 10.3892/mmr.2016.5720. Epub 2016 Sep 6.

Hydroxysafflor yellow A exerts antioxidant effects in a rat model of traumatic brain injury

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Hydroxysafflor yellow A exerts antioxidant effects in a rat model of traumatic brain injury

Yang Wang et al. Mol Med Rep. 2016 Oct.

Abstract

Free radical-induced oxidative damage occurs rapidly and is of primary importance during the secondary pathophysiological cascades of traumatic brain injury (TBI). Hydroxysafflor yellow A (HSYA) is a constituent of the flower petals of Carthamus tinctorius (safflower) and may represent a potential therapeutic strategy to improve outcomes following TBI. The present study aimed to identify HSYA in the brain tissues of rats exposed to TBI to determine its absorption and to investigate the underlying effects of HSYA on antioxidant enzymes in the brain tissues of TBI rats. To determine the absorption of HSYA for the investigation of the underlying antioxidant effects of HSYA in TBI, the presence of HSYA in the brain tissues of the TBI rats was identified using an ultra performance liquid chromatography‑tandem mass spectrometry method. Subsequently, the state of oxidative stress in the TBI rat model following the administration of HSYA was investigated by determining the levels of antioxidant enzymes, including superoxide dismutase (SOD), malondialdehyde (MDA) and catalase (CAT), and the ratio of glutathione (GSH)/glutathione disulfide (GSSG). The data obtained demonstrated that HSYA was absorbed in the brain tissues of the TBI rats. HSYA increased the activities of SOD and CAT, the level of GSH and the GSH/GSSG ratio. However, HSYA concomitantly decreased the levels of MDA and GSSG. These preliminary data suggest that HSYA has the potential to be utilized as a neuroprotective drug in cases of TBI.

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Figures

Figure 1
Figure 1
Chemical structure of hydroxysafflor yellow A.
Figure 2
Figure 2
Mass spectrum of hydroxysafflor yellow A.
Figure 3
Figure 3
Detection of HSYA in brain tissues of TBI rats using ultra-high performance liquid chromatography with tandem mass spectrometry. Representative multiple reaction monitoring chromatograms of HSYA in (A) untreated brain tissue, (B) normal brain tissue treated with reference HSYA and (C) brain tissue post-TBI and 30 min following intragastric administration of HSYA (30 mg/kg). HYSA, hydroxysafflor yellow A; TBI traumatic brain injury.
Figure 4
Figure 4
Effects of HSYA (10 and 30 mg/kg) on the levels of MDA in rat brain tissues at different time points. Values are expressed as the mean ± standard deviation. #P<0.01, compared with the sham group at the same time point, *P<0.05, compared with the vehicle group at the same time point, **P<0.01, compared with the vehicle group at the same time point. HYSA, hydroxysafflor yellow A; MDA, malondialdehyde.
Figure 5
Figure 5
Effects of HSYA (10 and 30 mg/kg) on the levels of SOD and CAT. The levels of (A) SOD and (B) CAT in the rat brain tissues were examined at different time points. Values are expressed as the mean ± standard deviation. #P<0.01, compared with the sham group at the same time point; *P<0.05, compared with the vehicle group at the same time point; **P<0.01, compared with the vehicle group at the same time point. HYSA, hydroxysafflor yellow A; SOD, superoxide dismutase; CAT, catalase.

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