Ursodeoxycholic acid protects dopaminergic neurons from oxidative stress via regulating mitochondrial function, autophagy, and apoptosis in MPTP/MPP+-induced Parkinson’s disease

Peiminine Reduces ARTS-Mediated Degradation of XIAP by Modulating the PINK1/Parkin Pathway to Ameliorate 6-Hydroxydopamine Toxicity and α-Synuclein Accumulation in Parkinson’s Disease Models In Vivo and In Vitro

“…For example, naringenin can improve the expression of PINK1 to diminish cellular oxidative stress and restore MMP, thereby alleviating 6-OHDA-induced toxicity in SH-SY5Y cells and zebrafish models [60]. In an MPTP-induced PD model, ursodeoxycholic acid modulates the PINK1/parkin pathway to improve mitochondrial function, inhibit apoptosis, and enhance autophagy, thus protecting DA neurons against oxidative stress [61]. Celastrol activates mitophagy by enhancing the performance of PINK1, thus preventing DA neuron death [62].…”

Ursodeoxycholic acid as a potential alternative therapeutic approach for neurodegenerative disorders: Effects on cell apoptosis, oxidative stress and inflammation in the brain

“…Similar to the most frequently used toxin MPP + , rotenone is able to inhibit complex I of the mitochondrial electron transport chain ( Greenamyre et al, 2010 ), application of low dose of rotenone leads to degeneration of dopaminergic neurons ( Blesa et al, 2012 ); while SNP is a strong NO generator, which can cause mitochondrial dysfunction in dopaminergic cells ( Zhang and Zhao, 2003 ). Interestingly, the beneficial properties of UDCA are somewhat partially mediated by preventing mitochondrial dysfunction ( Abdelkader et al, 2016 ; Chun and Low, 2012 ; Qi et al, 2021 ). In particular, UDCA treatment modulates mitochondrial homeostasis perturbations caused by treatment with rotenone in the striatum of male rat ( Abdelkader et al, 2016 ), and prevents mitochondria-dependent programmed cell death in both SNP-induced human neuroblastoma cells ( Chun and Low, 2012 ) and MPP + -induced mice neuroblastoma cells ( Qi et al, 2021 ).…”

“…Interestingly, the beneficial properties of UDCA are somewhat partially mediated by preventing mitochondrial dysfunction ( Abdelkader et al, 2016 ; Chun and Low, 2012 ; Qi et al, 2021 ). In particular, UDCA treatment modulates mitochondrial homeostasis perturbations caused by treatment with rotenone in the striatum of male rat ( Abdelkader et al, 2016 ), and prevents mitochondria-dependent programmed cell death in both SNP-induced human neuroblastoma cells ( Chun and Low, 2012 ) and MPP + -induced mice neuroblastoma cells ( Qi et al, 2021 ).…”

“…With respect to inflammation, UDCA reduces the rotenone-induced NF-κB mRNA expression and TNF-α, IL-1β, and IL-10 levels. In the third in vitro study used MPP + -treated mouse neuroblastoma (neuro-2a) cells to examine the effects of UDCA on PD pathogenesis, and findings showed that UDCA improves cell viability and decreases cell death in MPP + -treated cells, inhibits ROS accumulation and ATP depletion in mouse neuroblastoma cells ( Qi et al, 2021 ).…”

Effects of Telmisartan, an AT1 receptor antagonist, on mitochondria-specific genes expression in a mouse MPTP model of Parkinsonism

“…Recently, AT1R and AT2R have been discovered in brain mitochondrial outer and inner membrane, respectively [19]. Alleviation of mitochondrial function was shown to decrease oxidative stress and reduced the incidences of apoptosis in various neurological disorders [20][21][22][23].…”