Vinpocetine regulates levels of circulating TLRs in Parkinson’s disease patients
The pathogenesis of Parkinson’s disease (PD) is complex; it includes mitochondrial dysfunction, oxidative stress, and neuroinflammation. Notably, Toll-like receptors (TLRs) may activate inflammatory or anti-inflammatory responses in Parkinson’s disease. Vinpocetine has been tested as an anti-inflammatory in both animal and in vitro research. Thus, it is important to test whether the anti-inflammatory properties of vinpocetine may have a protective effect in PD patients.
Eighty-nine Parkinson’s disease patients and 42 healthy controls were recruited for this study. All patients were randomly assigned to either the traditional therapy group (T PD group, n = 46) or the vinpocetine group (V PD group, n = 43), in a blinded manner. Both treatments were administered for 14 days.
Administration of vinpocetine reduced mRNA levels of TLR2/4, as well as protein levels of the downstream signalling molecules, MyD88 and NF-κB; moreover, it lowered the expression levels of serum inflammatory cytokines, TNF-α and MCP-1. Notably, vinpocetine increased TLR3 mRNA levels, as well as protein levels of the downstream signalling molecules TRIF-β and IRF-3, and serum levels of the anti-inflammatory cytokines IL-10 and IL-8. Furthermore, vinpocetine produced a robust increase in the Mini Mental State Examination score, compared to that achieved by using levodopa therapy.
Vinpocetine treatment may exhibit anti-inflammatory activity and alleviate cognitive impairment.
KeywordsParkinson’s disease TLRs Vinpocetine Neuroinflammation
The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: the National Natural Science Foundation of China (Grant No. 81300115) to Liang Shao.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interest.
All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
Informed consent was obtained from all individual participants included in the study.
- 9.Smith GA, Rocha EM, Rooney T, Barneoud P, McLean JR, Beagan J, Osborn T, Coimbra M, Luo Y, Hallett PJ, Isacson O (2015) A Nurr1 agonist causes neuroprotection in a Parkinson’s disease lesion model primed with the toll-like receptor 3 dsRNA inflammatory stimulant poly(I:C). PLoS One 10(3):e0121072CrossRefGoogle Scholar
- 10.Szilágyi G, Nagy Z, Balkay L, Boros I, Emri M, Lehel S, Márián T, Molnár T, Szakáll S, Trón L, Bereczki D, Csiba L, Fekete I, Kerényi L, Galuska L, Varga J, Bönöczk P, Vas A, Gulyás B (2005) Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study. J Neurol Sci 229-230:275–284CrossRefGoogle Scholar
- 14.Fan CK (2006) Phosphodiesterase inhibitors in airways disease. Eur J Pharmacol 533(1–3):110–117Google Scholar
- 21.Ruiz-Miyazawa KW, Pinho-Ribeiro FA, Zarpelon AC, Staurengo-Ferrari L, Silva RL, Alves-Filho JC, Cunha TM, Cunha FQ, Casagrande R, Verri WA Jr (2015) Vinpocetine reduces lipopolysaccharide-induced inflammatory pain and neutrophil recruitment in mice by targeting oxidative stress, cytokines and NF-κB. Chem Biol Interact 237:9–17CrossRefGoogle Scholar
- 29.Molnár P, Gaál L, Horváth C (1994) The impairment of long-term potentiation in rats with medial septal lesion and its restoration by cognition enhancers. Neurobiology (Bp) 2(3):255–266Google Scholar