The Neuroprotective Effects of Lithium Chloride in a Model of Photochemically Induced Stroke

The aim of the study was to investigate the neuroprotective properties of lithium chloride in a model of photochemically induced stroke in rats. Materials and Methods. The experimental work was conducted in the organoprotection laboratory for critical conditions at the V. A. Negovsky Research Institute of General Reanimatology, Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology. The study included 32 outbred Wistar rats, randomized into 2 equal groups: the NaCl (control) group, treated with physiological saline solution, and the LiCl group, which received a 4.2% lithium chloride solution (63 mg/kg). The solutions were administered intravenously 120 minutes after inducing a stroke. The ischemic stroke model was generated using photochemically induced thrombosis in cerebral sensorimotor cortex vessels. Neurological deficit was assessed using the «limb placement test». Ischemic lesion volume was measured using MRI (7 Tesla). Immunohistochemical analysis included markers for NeuN (survived mature neurons), Cas-3 (neuronal apoptosis), and Iba-1 (microglial activation). Statistical analysis was performed using the Shapiro–Wilk test, Student's t- test, and the Mann–Whitney U test with significance at p  < 0.05. Results. Lithium chloride infusion resulted in a 30% reduction in the ischemic lesion volume compared to the control group ( p  = 0.0236). The LiCl group showed an increase in signal intensity (relative units, RU) in the NeuN-positive neurons in the penumbra (80 RU vs 41 RU in the control group, p  = 0.0001), a 25% decrease in signal intensity in Cas-3-positive cells ( p  = 0.0008), and a 58% decrease in signal intensity in Iba-1-positive cells ( p  < 0.0001). Neurological deficit in the LiCl group was less detectable (NaCL vs LiCl: 9,8 ± 1,2 vs 12,5 ± 1,5 scores, respectively, p  < 0.0001). Conclusion. Lithium chloride demonstrated significant neuroprotective properties in a model of ischemic stroke, reducing the volume of damage and favoring the suppression of apoptosis and inflammation. The findings validate the potential of lithium chloride as a therapeutic agent for treatment of ischemic stroke, owing in particular to ability to modulate key pathogenic mechanisms of the disease. The results underscore the need for further clinical research to assess the efficacy and safety of lithium in medical practice.