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Cadmium (Cd) is a naturally occurring harmful metal that can cause damage to many different tissues and organs in the body. Antioxidant agents are frequently utilized to counteract the harmful impact of this heavy metal on the body. This research explores the neuroprotective role of β-caryophyllene (BCP) in Cd-induced toxicity. Male Wistar rats were categorized into five groups: control, BCP400, Cd, BCP200 +Cd, and BCP400 +Cd. BCP suppressed Cd-induced oxidative damage in brain tissue by regulating the Nrf2/HO-1/SIRT1 signaling pathway. Moreover, BCP alleviates Cd-induced behavioral alterations through SIRT1 activation. Cd increased TNF-α and IL-1β levels and decreased IL-10 levels in brain tissue, whereas BCP suppressed TLR-4/NF-κB/JNK signaling pathway and restored these cytokines to normal levels. In addition, Cd exposure led to increased BAX and Caspase 3 and decreased Bcl-2 levels in neurons, but these proteins approached normal levels thanks to BCP's anti-apoptotic properties. Furthermore, while Beclin-1 and LC3A/B expression levels were increased in neurons of Cd-exposed animals, BCP suppressed these expressions by activating the PI3K/Akt/mTOR signaling pathway. Histopathological, biochemical, and molecular analyses confirmed BCP reduces oxidative stress, inflammation, apoptosis, and autophagy caused by Cd-induced neurotoxicity by regulating various signaling pathways and strengthening the antioxidant defense system. Therefore, we believe that BCP has a high potential as a therapeutic agent against Cd-induced neurotoxicity.
Bolat et al. (Mon,) studied this question.