Evaluating Antioxidant Enzyme Parameters in Rats Treated with Berberine-Loaded Bovine Serum Albumin Nanoparticles and Scopolamine

Abstract Introduction/Objective Introduction: Berberine (BER) has garnered attention for its antioxidant properties demonstrated in various studies, showing its ability to scavenge or inhibit reactive oxygen species (ROS) and reactive nitrogen species (RNS), including nitric oxide, superoxide anion, and peroxynitrites. Methods/Case Report Methods: Forty-two male Wistar rats were randomly assigned to seven groups, each comprising 6 rats: Sham control (no treatment), BSA-NPs orally administered, BRB-NPs orally administered, SCO intraperitoneally injected, BER followed by SCO injection, BSA-NPs with SCO injection, and BER-NPs with SCO injection. Treatments were administered daily for 28 days. The cholinergic status was evaluated by assessing acetylcholinesterase (AChE) activity in brain homogenates, and brain homogenate Aβ-42 levels were measured using the ELISA technique. Additionally, brain prooxidant markers (NO, TBARS, XO), nonenzymatic antioxidants (GSH), and enzymatic antioxidants (GPx, GST, and SOD) were measured. Results (if a Case Study enter NA) Results: The study revealed that treatment with BRB NPs resulted in the lowest AChE activity and Aβ-42 levels. Scopolamine administration significantly increased brain NO, TBARS, and XO activity, accompanied by a progressive depletion in GSH content (p<0.05). Treatment with BRB-free or BSA decreased NO levels, while the BSA or BRB-NPs groups exhibited higher brain TBARS levels than the sham group. All treated groups exhibited similar activity to the sham control, except for the BSA-treated group. Furthermore, all treated groups showed comparable GSH levels to the sham control, except for the scopolamine group. Treatment with BRB NPs normalized GPx activity and showed the highest GST activity. The BRB-NPs treated group also exhibited the highest SOD level. The p-value was <0.001 among all studied groups. Conclusion Conclusion: Injection of SCO induced oxidative impairments in brain tissue, evidenced by increased prooxidants such as NO and depletion of antioxidant capacity (GPx, GST, and GSH). SCO also disrupted glutathione metabolism, enhancing the level of lipid peroxidation in the brain. Treatment with BRB-NPs or free BRB progressively increased antioxidant capacity and mitigated the harmful effects of oxidative damage in the brain by reducing prooxidant levels.