Ganoderma lucidum stimulates autophagy-dependent longevity pathways in Caenorhabditis elegans and human cells

Abstract

The medicinal fungus Ganoderma lucidum is used as a dietary supplement and health tonic, but whether it affects longevity remains unclear. We show here that a water extract of G. lucidum mycelium extends lifespan of the nematode Caenorhabditis elegans . The G. lucidum extract reduces the level of fibrillarin (FIB-1), a nucleolar protein that correlates inversely with longevity in various organisms. Furthermore, G. lucidum treatment increases expression of the autophagosomal protein marker LGG-1, and lifespan extension is abrogated in mutant C. elegans strains that lack atg-18 , daf-16 , or sir-2.1 , indicating that autophagy and stress resistance pathways are required to extend lifespan. In cultured human cells, G. lucidum increases concentrations of the LGG-1 ortholog LC3 and reduces levels of phosphorylated mTOR, a known inhibitor of autophagy. Notably, low molecular weight compounds (<10 kDa) isolated from the G. lucidum water extract prolong lifespan of C. elegans and the same compounds induce autophagy in human cells. These results suggest that G. lucidum can increase longevity by inducing autophagy and stress resistance.

Eucommia ulmoides male flower as a remarkable edible floral resource exerts lifespan/healthspan-promoting effects on Caenorhabditis elegans

“…16 The intestinal lipofuscin accumulation level in wild-type nematodes was determined by the study of Vayndorf et al 17 Moreover, we used the TJ356, DA2123, and CF1553 strains to observe the intracellular localization of DAF-16 and compare the expression of LGG-1 and SOD3, respectively. 18–20 For mitophagy detection, the IR1511 strain was used, which expressed GFP-tagged DCT-1 and red fluorescent protein (DsRed)-tagged LGG-1 in body-wall muscles. The colocalization of two signals indicates the fusion of mitochondria with the lysosome, that is, the occurrence of mitophagy.…”

“…Food & Function localization of DAF-16 and compare the expression of LGG-1 and SOD3, respectively. [18][19][20] For mitophagy detection, the IR1511 strain was used, which expressed GFP-tagged DCT-1 and red fluorescent protein (DsRed)-tagged LGG-1 in body-wall muscles. The colocalization of two signals indicates the fusion of mitochondria with the lysosome, that is, the occurrence of mitophagy.…”

mTOR Complex 1 Content and Regulation Is Adapted to Animal Longevity

“…Remarkably, when injected intraperitoneally, reduced organismal mTOR signalling has been reported after only 1 h [ 53 ]. The reduced mTOR activity occurs along with an enhanced longevity [ 36 , 50 , 51 , 53 , 54 , 55 , 56 ]. Interestingly, rapamycin reduces mTOR activity and increases longevity in a dose-dependent manner [ 50 ] ( Table 4 ).…”

“…The molecular mechanisms through which rapamycin extends longevity and delays ageing are diverse, and include reduced ROS production at complex I, protein and lipid oxidation, and mitochondrial DNA alteration, along with enhanced mitochondrial biogenesis, stress resistance, autophagy and modulation of lipid metabolism [ 36 , 50 , 51 , 54 , 55 ]. The effects on protein translation and chromatin structure are complex.…”

(±)-Spiroganoapplanin A, a complex polycyclic meroterpenoid dimer from Ganoderma applanatum displaying potential against Alzheimer's disease

“…11 Ganoderma has been widely used as an edible and medicinal mushroom in China for about 2000 years. 12 The ancient Chinese agronomy book Shennong's Herbal Classic and Compendium of Materia Medica described the medical benefits of Ganoderma such as prolonging life-span, keeping health, improving intelligence and memory. 13 Modern pharmacological research studies have also provided evidence of the possible therapeutic effects of Ganoderma and its extracts on AD through inhibiting inflammation, resisting oxidation pressure and reducing the aggregation of Aβ.…”