S-allyl-l-cysteine ameliorates sensorimotor functions after intracerebral hemorrhage in mice concomitantly with prevention of axon tract fragmentation and reduction of brain lesion volume.

Abstract

Intracerebral hemorrhage (ICH) is a devastating type of stroke with high mortality and limited treatment options. Brain tissue injury featured by neuroinflammation and axonal damage plays a pivotal role in poor outcome. S-allyl-l-cysteine, a garlic-derived amino acid derivative, possesses antioxidant and anti-inflammatory properties and has been shown to afford neuroprotection in ischemic stroke models. In the present study, ICH was induced in male ICR mice by collagenase injection into the striatum. When S-allyl-l-cysteine (300 or 600 mg/kg) was administered intraperitoneally at 1 h before and 3, 27, and 51 h after ICH induction, the compound alleviated ICH-induced motor deficits as revealed by limb-placing and beam-walking tests in a dose-dependent manner. At 600 mg/kg, S-allyl-l-cysteine significantly suppressed hematoma-associated microglial/macrophage activation and neuronal loss, reduced axonal fragmentation in the internal capsule and decreased brain lesion volume, while having no effect on several other events such as astrocyte activation, nitrosative stress, or hemorrhage volume. S-allyl-l-cysteine also tended to inhibit neutrophil infiltration but did not alter expression of IL-6 and CXCL2 mRNAs. Overall, S-allyl-l-cysteine ameliorated prognosis of ICH, and the underlying mechanisms may involve suppression of microglial/macrophage activation and neuronal loss, attenuation of axonal injury, and reduction of brain lesion volume.