Beneficial effect of honokiol on lipopolysaccharide induced anxiety-like behavior and liver damage in mice

• Anxiety disorders are co-morbid neuropsychiatric disorder with inflammatory diseases.
• HNK pre-treatment attenuated LPS induced anxiety-like behavior & liver damage in mice.
• LPS induced elevated plasma IL-1β, IL-6, and TNF-α level were reversed by HNK.
• Decreased plasma BDNF level was improved by HNK pre-treatment in LPS challenged mice.
• Pre-treatment of HNK prevented LPS evoked liver oxidative stress and TNF-α activity.

Anxiety disorders are commonly occurring co-morbid neuropsychiatric disorders with chronic inflammatory conditions such as live damage. Numerous studies revealed that peripheral inflammation, oxidative stress and brain derived neurotrophic factor (BDNF) play important roles in the pathophysiology of anxiety disorders. Honokiol (HNK) is a polyphenol, possessing multiple biological activities including antioxidant, anti-inflammatory, anxiolytic, antidepressant and hepatoprotection. The present study was designed to investigate the effect of HNK, in lipopolysaccharide (LPS)-induced anxiety-like behavior and liver damage in mice. Mice (n = 6–10/group) were pre-treated with different doses of HNK (2.5 and 5 mg/kg; i.p.) for two days, and challenged with saline or LPS (0.83 mg/kg; i.p.) on third day. Anxiety-like behavior was monitored using elevated plus maze (EPM) and open field test (OFT). Animals were sacrificed to evaluate various biochemical parameters in plasma and liver. HNK pre-treatment provided significant (P < 0.01) protection against LPS-induced reduction in body weight, food and water intake in mice. HNK at higher dose significantly (P < 0.05) attenuated LPS-induced anxiety-like behavior by increasing the number of entries and time spent in open arm in EPM test, and by increasing the frequency in central zone in OFT. HNK pre-treatment ameliorated LPS-induced peripheral inflammation by reducing plasma IL-1β, IL-6, TNF-α level, and also improved the plasma BDNF level, prevented liver damage via attenuating transaminases (AST, ALT), liver oxidative stress and TNF-α activity in LPS challenged mice. In conclusion, the current investigation suggests that HNK provided beneficial effect against LPS-induced anxiety-like behavior and liver damage which may be governed by inhibition of cytokines production, oxidative stress and depletion of plasma BDNF level. Our result suggests that HNK could be a therapeutic approach for the treatment of anxiety and other neuropsychiatric disorders associated with inflammation and oxidative stress.

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