bims-metalz Biomed News
on Metabolic causes of Alzheimer’s disease
Issue of 2024–03–24
two papers selected by
Mikaila Chetty, Goa University
  1. Leaf extract of Garcinia atroviridis promotes anti-heat stress and antioxidant effects in Caenorhabditis elegans.
  2. VDR and deubiquitination control neuronal oxidative stress and microglial inflammation in Parkinson's disease.
  1. Front Pharmacol. 2024 ;15 1331627
    Leaf extract of Garcinia atroviridis promotes anti-heat stress and antioxidant effects in Caenorhabditis elegans.
    Sirithip Chuaijit, Chuchard Punsawad, Veronica Winoto, Waluga Plaingam, Itti Kongkaew, Atidtaya Phetcharat, Takafumi Ichikawa, Makoto Kubo, Fumitaka Kawakami, Aman Tedasen, Moragot Chatatikun.
      Introduction:Garcinia atroviridis has been used for traditional medicines, healthy foods and tea. The chemical compositions and biological activities of fruit, stem bark and root have been widely studied. However, the phytochemical components and the biological activities in Garcinia atroviridis leaves (GAL) are limited. This research aims to study the phytochemical components and the stress resistance effects of GAL in Caenorhabditis elegans (C. elegans). Methods: To investigate the chemical components and antioxidant activities of GAL extract, the ethanol extract was characterized by liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-QTOF MS) analysis and C. elegans was used to evaluate the effects of GAL extracts on longevity and stress resistance. Results and discussion: The results revealed that the ethanol extract of GAL possesses free radical scavenging activities. Furthermore, GAL extract increased the lifespan of C. elegans by 6.02%, 15.26%, and 12.75% at concentrations of 25, 50, and 100 μg/mL, respectively. GAL extract exhibited improved stress resistance under conditions of heat and hydrogen peroxide-induced stress. The survival rates of GAL extract-treated worms were significantly higher than those of untreated worms, and GAL extract reduced reactive oxygen species (ROS) accumulation. Additionally, GAL extract treatment upregulated the expression of stress resistance-associated genes, including gst-4, sod-3, skn-1, and hsp16.2. GAL extract supplementation alleviated stress and enhanced longevity by inducing stress-related genes in C. elegans. The observed effects of GAL extracts may be attributed to the stimulation of oxidant enzymes mediated through DAF-16/FOXO and SKN-1/NRF2, as well as the enhancement of thermal defense in C. elegans. Collectively, this study provides the first evidence of the antioxidant activities of GAL and elucidates the underlying mechanisms of stress resistance.
    Keywords:  Caenorhabditis elegans; Garcinia atroviridis; antioxidants; longevity; oxidative stress
    DOI:  https://doi.org/10.3389/fphar.2024.1331627
  2. Cell Death Discov. 2024 Mar 21. 10(1): 150
    VDR and deubiquitination control neuronal oxidative stress and microglial inflammation in Parkinson's disease.
    Zihui Zheng, Miao Chen, Shengliang Feng, Huanhuan Zhao, Tiange Qu, Xudong Zhao, Qinli Ruan, Lei Li, Jun Guo.
      Close correlation between vitamin D (VitD) deficiency and Parkinson's Disease (PD) risk, VitD as an adjuvant treatment promising to improve PD progression. However, VitD excessive intake could induce hypercalcemia and renal damage. Therefore, upregulation of vitD receptor (VDR) is considered a compensatory strategy to overcome VitD insufficiency and alleviate PD symptoms. In this study, we discovered that VDR played antioxidative roles in dopaminergic neurons by decreasing reactive oxygen species (ROS) and maintaining mitochondrial membrane potential. Further, we newly identified VDR downstream events in C. elegans, including glutathione S-transferase (gst) and forkhead box transcription factor class O (daf-16) mediated oxidative stress resistance. VDR upregulation also mitigated microglial activation through inhibition of NLRP3/caspase-1-mediated inflammation and membrane permeabilization. These findings highlight the multifaceted protective effects of VDR in both neurons and microglia against the development of PD. Importantly, we discovered a novel deubiquitinase DUB3, whose N-terminal catalytic domain interacted with the C-terminal ligand-binding domain of VDR to reduce VDR ubiquitination. Identification of DUB3 as an essential player in the deubiquitinating mechanism of VDR provides valuable insights into VDR regulation and its potential as a therapeutic target for PD.
    DOI:  https://doi.org/10.1038/s41420-024-01912-9
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