Background/Objectives: Intracerebral hemorrhage (ICH) is a severe subtype of stroke characterized by extensive secondary brain injury driven by oxidative stress, inflammation, and progressive neuronal loss, leading to poor neurological outcomes. Thymoquinone, a bioactive compound derived from Nigella sativa, has demonstrated potent antioxidant and neuroprotective properties, but its integrated effects in hemorrhagic stroke remain insufficiently explored. This study aimed to evaluate the antioxidant and neuroregenerative effects of thymoquinone in a rat model of ICH. Methods: Male Wistar rats with experimentally induced ICH were randomized into untreated controls and two treatment groups receiving thymoquinone (150 mg/kg and 250 mg/kg) for three consecutive days. Oxidative injury and antioxidant responses were assessed using membrane blebbing, malondialdehyde (MDA), superoxide dismutase (SOD) activity, and nuclear factor erythroid 2–related factor 2 (Nrf2) expression, while neuroprotection was evaluated by neuronal counts in perihematomal tissue. Results: Thymoquinone treatment significantly reduced membrane blebbing and MDA levels, while markedly increasing SOD activity and Nrf2 expression in a dose-dependent manner. These biochemical improvements were accompanied by significant preservation of neuronal morphology and increased neuronal survival, with the 250 mg/kg dose showing the strongest effects. Conclusions: In conclusion, thymoquinone confers robust antioxidant and neuroprotective benefits in experimental ICH and represents a promising candidate for mitigating secondary brain injury following intracerebral hemorrhage.