Abstract
Intracerebral hemorrhage (ICH) is a severe cerebrovascular disease with a high incidence, mortality and disability rate. Danhong injection (DHI) is beneficial for ischemic stroke, but is prohibited for ICH due to risk of bleeding. The present study aims to explore the potential therapeutic time window and molecular mechanism of DHI in a collagenase-induced ICH model in aged rats. DHI administration after ICH could significantly improve body weight and neurological deficits, and reduce the hematoma volume and brain water content when compared to the vehicle control. Furthermore, the protective effect of DHI administration on days 1–3 after ICH was superior to those on days 3–5 or 7–9 after ICH. DHI remarkably increased the Peroxiredoxin 1 (Prx1) expression in astrocytes and reduced the expression of inflammatory factors tumor necrosis factor-α (TNF-α) and interleukin-β (IL-1β) after ICH. The immediate treatment of Prx1 inhibiter chelerythrine (Che) after ICH abolished the protective effect of DHI. Furthermore, the Che treatment reduced the expression of Prx1 in astrocytes, but increased the expression of TNF-α and IL-1β after ICH. DHI treatment could not reverse these changes. Therefore, the earlier DHI is administered, the better the neuroprotective effect. DHI exerts antioxidative and anti-inflammatory function by increasing Prx1 in astrocytes. These present results may change the established understanding of DHI, and reveal a novel treatment approach for ICH.
Highlights
Intracerebral hemorrhage (ICH) is a catastrophic disease that causes severe disability and high mortality in adults
The present study is the first to demonstrate that Danhong injection (DHI) can be used to treat ICH, and that this has an outstanding neuroprotective effect on ICH
The earlier administration of DHI led to its better ability to promote neurological function and hematoma recovery
Summary
Intracerebral hemorrhage (ICH) is a catastrophic disease that causes severe disability and high mortality in adults. The cascading events induced by ICH are the main cause of secondary damage (Ironside et al, 2019). Oxidative stress and inflammation have been recognized as the major disruptive factors after ICH (Wang, 2010; Hu et al, 2016). Approaches that could inhibit oxidative stress and/or inflammation can reduce hematoma volume and promote neurological recovery after ICH (Wang et al, 2018)
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