A polysaccharide from Tetrastigma hemsleyanum Diels & Gilg alleviates experimental colitis by restoring AMPK-TFAM-associated mitochondrial DNA quality control
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Published on: February 27, 2014
Liu Yang1, Menghan Yang1, Xiaorong Hu1
1School of Medical Technology and Information Engineering, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.
Ethnopharmacological Relevance:
Tetrastigma hemsleyanum Diels & Gilg (Sanyeqing) is used in Chinese folk medicine for febrile and inflammatory disorders. Its polysaccharide fraction has shown intestinal protective activity, but the mitochondrial mechanism remains unclear.
Aim Of The Study:
To determine whether a chemically and structurally characterized T. hemsleyanum polysaccharide (THP) alleviates experimental colitis in association with improved mitochondrial DNA (mtDNA) homeostasis and mitochondrial quality-control responses.
Materials And Methods:
THP was purified and characterized by chromatographic, spectroscopic, and compositional analyses. Its effects were examined in dextran sulfate sodium-induced acute colitis in mice and lipopolysaccharide/tert-butyl hydroperoxide-injured Caco-2 cells. Mucosal injury, barrier function, mitochondrial redox status and respiration, cytosolic mtDNA, TFAM distribution, autophagy-lysosome-related markers, and AMPK-PGC1α-NRF1-TFAM and cGAS-STING signaling were evaluated. Dorsomorphin and bafilomycin A1 were used to assess the contribution of AMPK signaling and lysosome-dependent autophagic flux.
Results:
THP reduced disease activity, histological injury, inflammatory cytokines, and barrier disruption. It lowered cellular and mitochondrial ROS, improved mitochondrial morphology, membrane potential, respiration, and ATP production, and reduced cytosolic mtDNA accumulation. THP increased AMPK-PGC1α-NRF1-TFAM-related signaling and increased the spatial association of TFAM-positive mitochondrial material with LC3- and LAMP1-positive structures. Dorsomorphin or bafilomycin A1 attenuated several THP-associated effects. THP also reduced cGAS-STING, NF-κB, and NLRP3 pathway activation.
Conclusions:
THP ameliorated experimental colitis in association with improved mitochondrial redox and bioenergetic function, preservation of mtDNA homeostasis, and AMPK-TFAM-related mitochondrial quality control. The data support autophagy-lysosome involvement in the handling of TFAM-positive mtDNA-containing mitochondrial material, but do not establish selective nucleoid degradation. These findings support further investigation of THP as a mitochondria-targeted intestinal protective polysaccharide.