Polyphenols from Toona sinensis seeds alleviate neuroinflammation in rats with Parkinson's disease. - GreenMedInfo Summary

Objective To explore the inhibitory effects of polyphenols from Toona sinensis seeds (PTSS) on neuroinflammation and the underlying mechanism in rats with Parkinson's disease (PD). Methods PD rat models were prepared by stereotaxic injection of 6-hydroxydopamine (6-OHDA) into one side of striatum of Sprague-Dawley male rats. Model rats were randomly divided into model group and PTSS group (n=10), and a normal control group was set as well (n=10). The rotational behavior of rats was induced by intraperitoneal injection of apomorphine (APO) after 30 days, and the behavioral changes of rats from each group were investigated. The morphological and quantity changes of DA neurons (tyrosine hydroxylase positive, TH-positive), microglia cells (ionized calcium binding adaptor molecule-1, Iba1-positive) and astrocytes (glial fibrillary acidic protein, GFAP-positive) in substantia nigra (SN) of rats from each group were examined by immunohistochemistry. Inducible nitric oxide synthase (iNOS), nuclear factor-κB p65 (NF-κBp65), p38 mitogen-activated protein kinase (p38MAPK) and phosphor-p38 mitogen-activated protein kinase (p-p38MAPK) levels were evaluated through immunohistochemical staining. The protein levels of TH, GFAP, p38MAPK and p-p38MAPK in SN were examined by Western blot analysis. Results The number of rotations in the rats of the PTSS group was significantly reduced compared with that in the model group. The number of TH-positive cells in the model group was much less than that in the control group. The number and protein levels of TH-positive cells were enhanced significantly by PTSSintervention. Compared with the control group, the protein levels of Iba1, GFAP, iNOS, NF-κB, p38MAPK and p-p38MAPK in the injured side of the model group significantly increased, which could be suppressed significantly by PTSS intervention. Conclusion PTSS demonstrates protective effects on DA neurons by inhibiting p38MAPK signaling pathway and reducing the expression of inflammatory factors in PD rats.