Curcumin nanogel and its efficacy against oxidative stress and inflammation in rat models of ischemic stroke

<b>Aim:</b> The study was designed to develop and analyze curcumin nanoparticles. <b>Methods:</b> Curcumin nanoparticles were formulated and evaluated. Their efficacy in protecting against brain damage was investigated in a rat model of ischemic stroke, considering motor function, muscle strength and antioxidant enzyme activity. <b>Results:</b> Curcumin nanoparticles displayed a zeta potential of -55 ± 13.5 mV and an average particle size of 51.40 ± 21.70 nm. In ischemic stroke rat models, curcumin nanoparticle treatment significantly improved motor functions, and muscle strength and increased the activities of antioxidant enzymes like glutathione peroxidase, glutathione, glutathione S-transferase, superoxide dismutase and catalase, reducing oxidative stress and inflammation. <b>Conclusion:</b> Curcumin nanoparticles showed significant neuroprotective effects in ischemic stroke models. Ischemic stroke and neurodegenerative diseases: Ischemic stroke and neurodegenerative diseases share oxidative stress and inflammation pathways. The role of oxidative stress: Reperfusion of cerebral blood flow in ischemic stroke increases the generation of reactive oxygen species and exacerbates brain damage. The therapeutic potential of curcumin: Curcumin offers anti-inflammatory and antioxidant benefits for neurodegenerative diseases. Challenges in using curcumin: Despite its potential, the clinical application of curcumin is limited by its poor bioavailability, rapid metabolism and chemical instability. These challenges require innovative delivery methods to improve its therapeutic efficacy. Nanotechnology and curcumin: Nanotechnology offers a solution to the limitations of curcumin by improving its solubility, stability and bioavailability. Curcumin nanoparticles (CNP), especially when administered in the form of nanoparticles, showed improved preventive and therapeutic effects in neurodegenerative diseases. Physicochemical properties: CNP particles are designed to be dispersible in water without surfactants, indicating their suitability for injectable formulations. Their size, zeta potential and stability are critical for efficiently targeting the brain and crossing the blood–brain barrier. Behavioral and biochemical effects: CNP shows neuroprotective effects in rat models and improves motor function and muscle strength. It also reduces oxidative stress by enhancing the activity of antioxidant enzymes and molecules such as glutathione peroxidase, glutathione, glutathione S-transferases, superoxide dismutase and catalase. Modulation of antioxidant enzymes: CNP treatment increases essential antioxidants that protect against oxidative stress and inflammation in the brain. This also includes a significant increase in glutathione levels and the activities of enzymes crucial for detoxifying harmful substances. Effects on neuroinflammation and oxidative damage: By modulating antioxidant defenses, CNP can potentially reduce the effects of neuroinflammation and oxidative damage, which are central to the pathology of ischemic stroke and neurodegenerative diseases. Future directions and conclusion: The results suggest CNP may offer a novel therapeutic approach for ischemic stroke and related diseases. Further research is needed to understand the exact mechanisms of action, optimize dosing and explore applications in other models and diseases, which could revolutionize treatment strategies for stroke.