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Article: Cathepsin-B dependent autophagy ameliorates steatoheaptitis in chronic exercise rats

TitleCathepsin-B dependent autophagy ameliorates steatoheaptitis in chronic exercise rats
Authors
KeywordsAerobic exercise
Autophagosome
lysosomal membrane
Oxidative stress
Apoptosis
Issue Date2020
PublisherUniversidad de Murcia, Departamento de Biologia Celular e Histologia. The Journal's web site is located at http://www.hh.um.es
Citation
Histology and Histopathology: From Cell Biology to Tissue Engineering, 2020, v. 35 n. 8, p. 833-847 How to Cite?
AbstractSummary. Purpose. This study aimed to investigate the role of cathepsin B dependent autophagy induced by chronic aerobic exercise on a high-fat diet (HFD)-induced nonalcoholic steatohepatitis (NASH) in rats. Methods. Healthy female (Sprague-Dawley) SD rats (8-10 weeks old; 180g-200g; n=6 per group) were divided into: (1) control group; (2) HFD group; (3) Exercise group; (4) HFD + exercise group. Rats were fed with a normal chow or an HFD for 12 weeks. Rats with exercise ran on a rotarod for 30 min per day from weeks 9-12. Results. Exercise training significantly (1) upregulated the levels of autophagy markers Beclin1, ATG5 and LC3II partly through inhibiting the p-AKT/mTOR pathway; (2) ameliorated HFD-mediated accumulation of fat mass by upregulating β-oxidation regulator PPAR-α and downregulating fatty acid synthesis marker SREBP-1c via lipophagy; (3) diminished the HFD-induced hepatic pro-inflammatory mediators TNF-α and IL-1β via NF-κB inactivation; (4) decreased the NASH-induced hepatic apoptotic marker caspase-3 activation caused by the upstream oxidative stress and by cytochrome P450 2E1 (CYP2E1); (5) mitigated the HFD-mediated lysosomal membrane permeabilisation and cathepsin B release partly via the reduction of reactive oxygen species (ROS). Conclusions. Chronic aerobic exercise reduces oxidative stress/ROS and ROS may cause lysosomal membrane destabilisation and disrupts the autophagic process. The beneficial effect of chronic exercise may further inhibit the process of lysosome membrane permeabilisation and facilitate lysosome fusion with autophagosomes to trigger autophagy. This process may possibly contribute to the inhibition of cathepsin B released into cytosol which further reduces inflammation and mitochondrial-dependent apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/288411
ISSN
2020 Impact Factor: 2.303
2020 SCImago Journal Rankings: 0.628
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGuo, R-
dc.contributor.authorYu, Q-
dc.contributor.authorLiong, EC-
dc.contributor.authorFung, ML-
dc.contributor.authorTipoe, GL-
dc.date.accessioned2020-10-05T12:12:29Z-
dc.date.available2020-10-05T12:12:29Z-
dc.date.issued2020-
dc.identifier.citationHistology and Histopathology: From Cell Biology to Tissue Engineering, 2020, v. 35 n. 8, p. 833-847-
dc.identifier.issn0213-3911-
dc.identifier.urihttp://hdl.handle.net/10722/288411-
dc.description.abstractSummary. Purpose. This study aimed to investigate the role of cathepsin B dependent autophagy induced by chronic aerobic exercise on a high-fat diet (HFD)-induced nonalcoholic steatohepatitis (NASH) in rats. Methods. Healthy female (Sprague-Dawley) SD rats (8-10 weeks old; 180g-200g; n=6 per group) were divided into: (1) control group; (2) HFD group; (3) Exercise group; (4) HFD + exercise group. Rats were fed with a normal chow or an HFD for 12 weeks. Rats with exercise ran on a rotarod for 30 min per day from weeks 9-12. Results. Exercise training significantly (1) upregulated the levels of autophagy markers Beclin1, ATG5 and LC3II partly through inhibiting the p-AKT/mTOR pathway; (2) ameliorated HFD-mediated accumulation of fat mass by upregulating β-oxidation regulator PPAR-α and downregulating fatty acid synthesis marker SREBP-1c via lipophagy; (3) diminished the HFD-induced hepatic pro-inflammatory mediators TNF-α and IL-1β via NF-κB inactivation; (4) decreased the NASH-induced hepatic apoptotic marker caspase-3 activation caused by the upstream oxidative stress and by cytochrome P450 2E1 (CYP2E1); (5) mitigated the HFD-mediated lysosomal membrane permeabilisation and cathepsin B release partly via the reduction of reactive oxygen species (ROS). Conclusions. Chronic aerobic exercise reduces oxidative stress/ROS and ROS may cause lysosomal membrane destabilisation and disrupts the autophagic process. The beneficial effect of chronic exercise may further inhibit the process of lysosome membrane permeabilisation and facilitate lysosome fusion with autophagosomes to trigger autophagy. This process may possibly contribute to the inhibition of cathepsin B released into cytosol which further reduces inflammation and mitochondrial-dependent apoptosis.-
dc.languageeng-
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histologia. The Journal's web site is located at http://www.hh.um.es-
dc.relation.ispartofHistology and Histopathology: From Cell Biology to Tissue Engineering-
dc.subjectAerobic exercise-
dc.subjectAutophagosome-
dc.subjectlysosomal membrane-
dc.subjectOxidative stress-
dc.subjectApoptosis-
dc.titleCathepsin-B dependent autophagy ameliorates steatoheaptitis in chronic exercise rats-
dc.typeArticle-
dc.identifier.emailYu, Q: lareina6@hku.hk-
dc.identifier.emailFung, ML: fungml@hku.hk-
dc.identifier.emailTipoe, GL: tgeorge@hku.hk-
dc.identifier.authorityFung, ML=rp00433-
dc.identifier.authorityTipoe, GL=rp00371-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.14670/HH-18-204-
dc.identifier.pmid31975365-
dc.identifier.scopuseid_2-s2.0-85082793608-
dc.identifier.hkuros315788-
dc.identifier.hkuros316108-
dc.identifier.volume35-
dc.identifier.issue8-
dc.identifier.spage833-
dc.identifier.epage847-
dc.identifier.isiWOS:000557879000007-
dc.publisher.placeSpain-
dc.identifier.issnl0213-3911-

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