Donny Wisnu Wardhana, Husnul Khotimah, Tommy Alfandy Nazwar, Nurdiana Nurdiana
Kastamonu Medical Journal - 2025;5(4):253-258
Aims: Traumatic brain injury (TBI) is a long-term disorder that results in lifelong disability, often in the form of cognitive impairment due to glial scar formation. Treatment with minocycline may reduce the transforming growth factor-beta-1 (TGF-beta1) pathway. Our assumption was that minocycline also contributed to the inhibition of glial scar via the TGF-beta1 pathway in TBI. The study aimed to assess how minocycline affects the TGF-beta1 signaling pathway in TBI model rats to inhibit the formation of glial scars. Methods: Twenty male Sprague Dawley rats were divided in five groups, with four rats per group. Day 0 of TBI using the weight drop model was followed by 14 days of minocycline treatment at doses of 25 mg/kg (MNO1 group), 50 mg/kg (MNO2 group), and 100 mg/kg (MNO3 group). On day 15, the novel object recognition (NOR) test was performed. On day 16, immunofluorescence double staining was carried out. Results: In rats with TBI models, minocycline inhibited the formation of glial scars. It has been demonstrated that minocycline inhibits the formation of TGF-beta1, which in effect inhibits the formation of glial scar in the perilesional area of TBI model rats. In TBI model rats, inhibition of glial scar may ameliorate cognitive function deficit. In TBI model rats, minocycline administration can improve cognitive function. Conclusion: Through the reduction of TGF-beta1 expression, minocycline inhibited glial scar formation in a rat model of TBI.
