Study on the potential neuroprotective effect of tetramethylpyrazine in rotenone-induced model of Parkinson’s disease in rats

Abstract

Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease, was originally described in 1817 by James Parkinson in the classic ‘‘Essay on the Shaking Palsy’’. All the cardinal signs of PD relate to motor dysfunction and include resting tremor, bradykinesia, rigidity and postural reflex impairment. Other manifestations include psychiatric symptoms such as anxiety and depression and dysautonomic symptoms such as hypotension and constipation, paresthesias, cramps, olfactory dysfunction, and seborrheic dermatitis. The main pathological finding associated with the motor deficits of PD is degeneration of the dopaminergic neurons of the pars compacta of the substantia nigra leading to loss of dopamine (DA) in the striatum. Symptoms do not develop until about 50–60% of the nigral neurons are lost and about 80–85% of the dopamine content of the striatum is depleted. Catecholaminergic and serotoninergic brain-stem neurons may also degenerate. Lewy bodies (LBs)—eosinophilic inclusion bodies containing many different proteins—are present mainly in the surviving neurons. α-synuclein is the major protein component present in LBs. The identification of several genes related to PD has provided clues about the molecular mechanisms involved in its pathogenesis. These mechanisms may include defective handling of misfolded proteins, mitochondrial dysfunction, oxidative stress, apoptosis and inflammation. Rotenone is a naturally occurring compound extracted