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Paeoniflorin mitigates high glucose-induced lifespan reduction by inhibiting insulin signaling in Caenorhabditis elegans
Summary
Researchers found that paeoniflorin, a natural plant compound, helped counteract the lifespan-shortening effects of high glucose exposure in the roundworm C. elegans by modulating insulin signaling pathways. While not directly about microplastics, this study is relevant because it explores protective mechanisms against environmental stressors at the cellular level. Understanding how natural compounds protect organisms from toxic exposures could inform research on mitigating microplastic-related harm.
In organisms, high glucose can cause several aspects of toxicity, including the lifespan reduction. Paeoniflorin is the major component of Paeoniaceae plants. Nevertheless, the possible effect of paeoniflorin to suppress high glucose toxicity in reducing lifespan and underlying mechanism are largely unclear. Thus, in this study, we examined the possible effect of paeoniflorin in suppressing high glucose (50 mM)-induced lifespan reduction and the underlying mechanism in <i>Caenorhabditis elegans</i>. Administration with 16-64 mg/L paeoniflorin could prolong the lifespan in glucose treated nematodes. Accompanied with this beneficial effect, in glucose treated nematodes, expressions of <i>daf-2</i> encoding insulin receptor and its downstream kinase genes (<i>age-1</i>, <i>akt-1</i>, and <i>akt-2</i>) were decreased and expression of <i>daf-16</i> encoding FOXO transcriptional factor was increased by 16-64 mg/L paeoniflorin administration. Meanwhile, the effect of paeoniflorin in extending lifespan in glucose treated nematodes was enhanced by RNAi of <i>daf-2</i>, <i>age-1</i>, <i>akt-1</i>, and <i>akt-2</i> and inhibited by RNAi of <i>daf-16</i>. In glucose treated nematodes followed by paeoniflorin administration, the increased lifespan caused by <i>daf-2</i> RNAi could be suppressed by RNAi of <i>daf-16</i>, suggesting that DAF-2 acted upstream of DAF-16 to regulate pharmacological effect of paeoniflorin. Moreover, in glucose treated nematodes followed by paeoniflorin administration, expression of <i>sod-3</i> encoding mitochondrial Mn-SOD was inhibited by <i>daf-16</i> RNAi, and the effect of paeoniflorin in extending lifespan in glucose treated nematodes could be suppressed by <i>sod-3</i> RNAi. Molecular docking analysis indicated the binding potential of paeoniflorin with DAF-2, AGE-1, AKT-1, and AKT-2. Therefore, our results demonstrated the beneficial effect of paeoniflorin administration in inhibiting glucose-induced lifespan reduction by suppressing signaling cascade of DAF-2-AGE-1-AKT-1/2-DAF-16-SOD-3 in insulin signaling pathway.
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