Zaafan M.A.Abdelhamid A.M.Ibrahim S.M.Pharmacology & Toxicology DepartmentFaculty of PharmacyMSA UniversityEgypt; Biochemistry DepartmentFaculty of PharmacyMSA UniversityEgypt2020-01-092020-01-09201913892010https://doi.org/10.2174/1389201020666190611122747PubMed ID 31198107https://t.ly/AZxY8ScopusObjective: Korean red ginseng was reported to have many biological effects like the antioxidant and the anti-inflammatory activities. Oxidative stress and neuro-inflammation play major roles in the pathogenesis of Parkinsons disease (PD). The current study aimed to investigate the protective effects of ginseng on rotenone-induced PD in rats. Methods: Rats were randomly allocated into 4 groups: Normal rats, rotenone control, ginseng+rotenone and ginseng only treated rats. The severity of PD was evaluated through locomotor activity perceived in the open field test, histological examination and immunohistochemical detection of amyloid-? in brain tissues, in addition to the biochemical assessment of tyrosine hydroxylase activity in brain tissues. Moreover, the following parameters were investigated for studying the possible mechanisms of ginseng neuroprotective effect: Nuclear factor-?? (NF-??), tumor necrosis factor-alpha (TNF-?), caspase- 3, lipid peroxides and reduced glutathione (GSH). Results: Ginseng exhibited potent neuroprotective effect that was reflected upon the histopathological examination, marked improvement in the locomotor activity and through its ability to suppress the amyloid-? deposition in the cortex and striatum along with significant increase in the tyrosine hydroxylase activity. Ginseng successfully inhibited the NF-?? inflammatory pathway in brain tissues beside the inhibition of other oxidative stress and inflammatory mediators. Furthermore, it exhibited antiapoptotic effect via the inhibition of caspase-3 expression. Conclusion: Ginseng could be a promising treatment in PD. It can suppress dopaminergic neuron degeneration through variable mechanisms mainly via inhibition of NF-?? pathway in addition to inhibition of oxidative stress and apoptosis. 2019 Bentham Science Publishers.EnglishAnti-oxidantCaspase-3GinsengNuclear factor-??Parkinsons diseaseRat modelamyloid beta proteinantiinflammatory agentantioxidantcaspase 3glutathione peroxidaseimmunoglobulin enhancer binding proteinkorean red ginsenglipid peroxidasemalonaldehydeplant extracttumor necrosis factortyrosine 3 monooxygenaseunclassified drugCasp3 protein, ratcaspase 3dopamineglutathioneimmunoglobulin enhancer binding proteinneuroprotective agentplant extractrotenoneanimal experimentanimal modelanimal tissueantiinflammatory activityArticlebrain diseasebrain hemorrhagebrain tissuecontrolled studydrug mechanismenzyme activityenzyme linked immunosorbent assayexperimental parkinsonismginsenggliosishistologyhistopathologyimmunohistochemistryimmunomodulationlocomotionmalemicroscopynerve cell degenerationneuroprotectionnonhumanopen field behavioropen field testoxidative stresspolymerase chain reactionprotein analysisprotein expressionpyknosisratvenous congestionanimalanimal behaviorapoptosischemistrydrug effectisolation and purificationmetabolismPanaxparkinsonismpathologyrandomizationSouth KoreaWistar ratAnimalsApoptosisBehavior, AnimalCaspase 3DopamineGlutathioneMaleNeuroprotective AgentsNF-kappa BOxidative StressPanaxParkinsonian DisordersPlant ExtractsRandom AllocationRats, WistarRepublic of KoreaRotenoneArticlehttps://doi.org/10.2174/1389201020666190611122747PubMed ID 31198107