Caffeic acid improves locomotor activity and lessens inflammatory burden in a mouse model of rotenone-induced nigral neurodegeneration: Relevance to Parkinson’s disease therapy

Will your doctor throw the kitchen sink at your stroke problems even if just suggested in a mouse model? Does your doctor try anything for your recovery that is not the status quo? The status quo is a complete failure, 10% almost full recovery. Is your doctor ok with that failure rate? 

You need to worry about Parkinsons.

Parkinson’s Disease May Have Link to Stroke

Caffeic acid improves locomotor activity and lessens inflammatory burden in a mouse model of rotenone-induced nigral neurodegeneration: Relevance to Parkinson’s disease therapy

Author links open overlay panelSawsan A.Zaitone^abEmanAhmed^cNehal M.Elsherbiny^deEman T.Mehanna^fMohammed K.El-Kherbetawy^gMohamed H.ElSayed^hDuha M.AlshareefⁱYasser M.Moustafa^b

https://doi.org/10.1016/j.pharep.2018.08.004Get rights and content

Abstract

Background

Caffeic acid phenethyl ester is found in honey bee propolis. It has immunomodulatory, anti-inflammatory and ant-cancer properties. Rotenone is a pesticide commonly used for inducing experimental Parkinson’s disease (PD) due to complex I inhibition and microglia activating properties. The current study examined neuroprotective effect of caffeic acid against rotenone-induced neurodegeneration in groups of seven mice.

Methods

Mice received protective doses of caffeic acid (2.5, 5 or 10 mg/kg) daily and nine injections of rotenone (1 mg kg, subcutaneously) - every 48 hours. Behavioral evaluation of motor function was done by a battery of tests including open-field test, cylinder test, pole test and rotarod test; all these tests showed motor impairment.

Results

Assay of striatal dopamine highlighted a significant decrease and increases in inflammatory markers. In addition, histopathological assessment of substantia nigra neurons demonstrated low immunostaining for tyrosine hydroxylase (TH) in rotenone treated mice. PCR analysis highlighted upregulation for genes encoding CD₁₁b (a microglia surface antigen), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and nuclear factor-κB (NFκB). Treatment with caffeic acid (5 or 10 mg/kg) amended most of rotenone-induced motor deficits, lessened microglia expression and inflammatory mediators and improved the nigral TH immunostaining.

Conclusion

These results confirmed the anti-inflammatory activity of caffeic acid and highlighted its neuroprotective activity against rotenone-induced neurodegeneration in mice.