Neuroprotective Effects of Curcuma longa and Rosmarinus officinalis Extracts on Oxidative Stress and Inflammation in the Brains of Alcohol-treated Rats

Background: Neurological disorders remain a global health challenge. Chronic alcohol consumption induces damage to the brain that can cause various forms of dementia. An abundance of acetaldehyde is produced by excessive alcohol consumption and accumulates in the body to induce oxidative stress, apoptosis, and inflammation in neuronal cells, which results in brain damage leading to memory loss. This study is aimed at investigating the effect of mixed ethanol extract of Curcuma longa rhizome and Rosmarinus officinalis leaf on oxidative stress and proinflammatory markers in the brain of alcohol- treated male Wistar rats. Methods: Twenty-five male Wistar rats were divided into five groups: control, mixed extract only (600 mg/kg), alcohol only (15 ml/kg of 40% ethanol), and mixed extract + alcohol groups at 300 mg/kg and 600 mg/kg doses. Treatments were administered orally for 21 days. Brain homogenates were analyzed for superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), reduced glutathione (GSH), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and AChE activity. Histopathological evaluations assessed neuroprotective effects. Results: Alcohol administration significantly decreased SOD (16.2 ± 1.3 U/mg protein), catalase (12.8 ± 0.9 U/mg protein), GPx (10.7 ± 0.8 U/mg protein), and GSH (9.2 ± 0.6 mg/g protein) compared to the control group (32.8 ± 2.2 U/mg, 23.5 ± 1.7 U/mg, 18.9 ± 1.2 U/mg, and 18.3 ± 1.1 mg/g, respectively; p<0.05). MDA levels increased to 7.6 ± 0.3 nmol/mg protein compared to 2.8 ± 0.2 nmol/mg in the control group. Treatment with 600 mg/kg of mixed extracts significantly restored SOD (31.5 ± 2.4 U/mg), catalase (22.6 ± 1.4 U/mg), GPx (17.8 ± 1.0 U/mg), GSH (17.4 ± 1.2 mg/g), and reduced MDA (3.2 ± 0.3 nmol/mg; p<0.05). TNF-α and IL-1β levels were elevated in alcohol-only rats (123.5 ± 4.3 pg/mL and 85.6 ± 3.2 pg/mL) compared to controls (68.3 ± 2.8 pg/mL and 43.2 ± 1.7 pg/mL, p<0.05) but were significantly reduced with mixed extract treatment. Histopathological analyses confirmed reduced neurodegeneration and restoration of normal brain architecture in treated groups. Conclusion: The mixed extract demonstrated significant neuroprotective effects by mitigating oxidative stress, inflammation, and neuronal damage in alcohol-treated rats. These findings suggest its potential as a therapeutic candidate for preventing alcohol-induced dementia.