Effects of Justicia carnea leaf extract on cerebral oxidative stress parameters and expression of cellular adhesion molecule-1 in albino mice exposed to TNBS

Abstract Background Although Justicia carnea possesses antioxidant qualities, its neuroprotective potential has not been well examined. Therefore, this study investigated the therapeutic potential of J. carnea extract in reducing tissue damage and oxidative stress brought on by exposure to 2,4,6-trinitribenzensulphurnic acid (TNBS) in albino mice. A total of 35 Swiss albino adult mice were split up into seven groups ( n = 5) and given a variety of treatments, such as normal saline (neutral control), TNBS (0.2 ml) intrarectally as a negative control, TNBS (0.2 ml) + sulfasalazine (500 mg/kg orally) as a positive control, and two different doses of J. carnea leaf extract (200 mg/kg and 400 mg/kg) given orally and intrarectally. The leaf of J. carnea was dried, extracted, and then formulated into a gel using sodium carboxymethyl cellulose (NaCMC) and glycerol. The animals received treatment for seven days before being sacrificed. Samples of blood and brain were gathered for immunohistochemical and biochemical examination. Results The findings demonstrated that TNBS significantly decreased glutathione (GSH) levels and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) while increasing C-reactive protein (CRP) levels, platelet counts, malonaldehyde (MDA), and nitric oxide (NO). On the other hand, Justicia carnea therapy successfully decreased platelet counts, MDA, CRP, and NO levels, especially at 400 mg doses. Additionally, it considerably ( P > 0.05) increased GSH levels and antioxidant enzymes activities. The extract’s neuroprotective and antioxidant properties were demonstrated by the considerable reduction in cellular adhesion molecule-1 (ICAM-1) expression as well as the mitigation of TNBS-induced cortical necrosis and neuronal degeneration. Conclusion The study showed that J. carnea leaf extract offers a substantial defense against tissue damage and brain oxidative stress brought on by TNBS.