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SARENG, H. R.

Publications and source records attributed to SARENG, H. R..

2 recordsLinked to original sources

Epoxyazadiradione ameliorates Parkinson's disease by upregulating heat shock factor 1 and protein degradation pathways in mice.

Parkinsons disease (PD) is a major debilitating health concern for millions of the elderly population all over the world. This progressive neurodegenerative disorder also poses a severe mental and financial burden to caregivers and society. Despite a major thrust on research for therapy development, no significant progress has been made; only temporary management options are currently available. To this end, we have reported azadiradione (AZD), a triterpenoid that we isolated from neem seed extract using a cell-based assay. AZD showed high efficacy in ameliorating protein aggregation-induced pathology and symptoms in fruit flies and mice. Current evidence suggests that AZD functions through activating the transcriptional function of heat shock factor 1 (HSF1), a master regulator of protein quality control pathways, without modulating the cellular redox balance. To better understand the pharmacophore of AZD, a triterpenoid in its observed function, we have analysed various structural derivatives, focusing on their HSF1-activating function in vitro and their efficacies in ameliorating protein aggregation-induced toxicities in cell and mouse models. Our analyses, based on real-time PCR, immunoblots, fluorescent anisotropy, and a mouse model of MPTP-induced PD, highlighted Epoxy-azadiradione (Epoxy) as being as efficient as AZD in in vivo functional tests, albeit activating the promoter binding activity of HSF1 with at least two-fold higher efficacy in vitro. Notably, similar to AZD, Epoxy did not induce cellular redox imbalance. We also incorporated molecular docking analyses involving the published crystal structure of the DNA-binding domain of HSF1 bound to its DNA recognition element to study molecular dynamics-based energy estimation. The analysis revealed a higher energy stability of the epoxy-bound complexes, as indicated by a significant decrease in binding free energy ({Delta}G) estimated from an ensemble of intermediate docked complex structures.

pharmacology and toxicology↗

HSF1 Activator Azadiradione Ameliorates Parkinson Disease and Extends Lifespan in Preclinical Models: Analysis of Underlying Molecular Mechanism

Parkinsons disease (PD) affects millions worldwide, with no efficient therapy currently available. A major cause of the initiation and progression of this degenerative disease is the dysfunctional cellular protein quality control system (PQC), leading to the accumulation of toxic protein aggregates in neurons. We previously reported azadiradione (AZD), a small molecule (MW 451 Da), as a potent inducer of heat shock factor 1 (HSF1) activity, which could alleviate cellular toxicity induced by misfolded proteins by upregulating the levels of inducible molecular chaperones and proteasome activity. Here, we show the multifaceted effect of AZD in enhancing the capacity of PQC machinery in cells, fruit flies, and a PD mouse model. AZD activated HSF1 by promoting its phosphorylation at S326 through MEK. In parallel, AZD boosted protein degradation through increased chymotrypsin-like proteasome activity, upregulation of the ubiquitin ligase CHIP. AZD induced autophagy, marked by elevated levels of Beclin 1, ATG7, and ULK1 phosphorylation at S555, along with mTORC1 inhibition via AMPK activation. Surprisingly, the calorie restriction pathway was also upregulated upon AZD treatment, as demonstrated by the enhanced phosphorylation of FOXO3 and FOXO1, along with increased activity of their target enzymes SOD and catalase. Notably, AKT activity was also suppressed in AZD-treated cells. In vivo, AZD improved motor function, dopaminergic neuron survival, and tyrosine hydroxylase activity in an MPTP-induced mouse model of PD, and extended lifespan in Drosophila without compromising fertility or mobility. These findings highlight AZD as a promising therapeutic candidate for restoring PQC and mitigating PD pathology.

molecular biology↗