Is lithium neuroprotective? An updated mechanistic illustrated review.

Neurodegeneration is a pathological process characterized by progressive neuronal impairment, dysfunction, and loss due to mitochondrial dysfunction, oxidative stress, inflammation, and apoptosis. Many studies have shown that lithium protects against neurodegeneration. Herein, we summarize recent clinical and laboratory studies on the neuroprotective effects of lithium against neurodegeneration and its potential to modulate mitochondrial dysfunction, oxidative stress, inflammation, and apoptosis. Recent findings indicate that lithium regulates critical intracellular pathways such as phosphatidylinositol-3 (PI3)/protein kinase B (Akt)/glycogen synthase kinase-3 (GSK3ß) and PI3/Akt/response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF). We queried PubMed, Web of Science, Scopus, Elsevier, and other related databases using search terms related to lithium and its neuroprotective effect in various neurodegenerative diseases and events from January 2000 to May 2022. We reviewed the major findings and mechanisms proposed for the effects of lithium. Lithium's neuroprotective potential against neural cell degeneration is mediated by inducing anti-inflammatory factors, antioxidant enzymes, and free radical scavengers to prevent mitochondrial dysfunction. Lithium effects are regulated by two essential pathways: PI3/Akt/GSK3ß and PI3/Akt/CREB/BDNF. Lithium acts as a neuroprotective agent against neurodegeneration by preventing inflammation, oxidative stress, apoptosis, and mitochondrial dysfunction using PI3/Akt/GSK3ß and PI3/Akt/CREB/BDNF signaling pathways.

Hepato-Protection Effect of Curcumin Against Methylphenidate-Induced Hepatotoxicity: Histological and Biochemical Evidences.

Background: As a psychostimulant agent, methylphenidate (MPH) abuse can cause serious liver damage. Studies have documented the hepatoprotective impacts of curcumin on liver damage. According to this definition, the purpose of this study is to explain the hapatoprotective effects of curcumin against the hepatotoxicity induced by MPH. Methods: Seventy rats were equally divided into seven groups (10 rats per group). Groups 1 and 2 received normal saline (0.7 mL/rat) and MPH (10 mg/kg), respectively for 21 days. Groups 3, 4, 5, and 6 concurrently received MPH (10 mg/ kg) and curcumin (10, 20, 40, and 60 mg/kg, respectively) for 21 days. Group 7 was treated with curcumin (60 mg/kg) alone for 21 days. The hepatic function test key enzymes such as AST, ALP, and histology of liver tissue (ALT), and alkaline phosphatase (ALP) levels was studied in the blood samples, and also, the histopathological changes and cell density changes were evaluated in the liver tissue. Results: The latest studies have shown that the administration of MPH induces rises in the AST, ALT, and ALP levels and induces degeneration changes in histopathology, whereas curcumin administration at doses of 40 and 60 mg/kg reduced the elevation of MPH-induced hepatic enzyme and inhibited histopathological degeneration in the MPH-treated classes. Curcumin alone (60 mg/kg) did not alter the biochemical and histological parameters. Conclusions: Curcumin can function as a hepatoprotective agent against MPH-induced hepatotoxicity.