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Hepatic histopathology and apoptosis in diet-induced-obese mice under Escherichia coli pneumonia
Author(s) -
Hetao Song,
Zhicai Zuo,
Zhuangzhi Yang,
Caixia Gao,
Kejie Chen,
Jing Fang,
Hengmin Cui,
Ping Ouyang,
Junliang Deng,
Yi Geng,
Hongrui Guo
Publication year - 2019
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.101956
Subject(s) - histopathology , apoptosis , adipokine , biology , oxidative stress , escherichia coli , medicine , endocrinology , glutathione , immunology , microbiology and biotechnology , pathology , obesity , biochemistry , leptin , enzyme , gene
This research was to investigate the difference of hepatic histopathology and apoptosis between the diet-induced obesity (DIO) and normal (lean) mice after Escherichia coli ( E. coli ) pneumonia. A total of 128 ICR mice were selected to be challenged intranasally with phosphate-buffered saline (PBS) or 4×10 9 CFUs/mL of E. coli , and the liver histopathology and apoptosis were examined pre- and post-infection. Results showed that the liver index, levels of lipid droplets, cytokines, adipocytokines, oxidative stress, apoptotic percentage, and apoptotic related factors in the E. coli- infected mice were generally higher than those in the uninfected mice, whereas the hepatic glycogen and Bcl-2 were the opposite. Interestingly, after E. coli infection, the DIO- E. coli mice exhibited decreased liver index and apoptotic percentages, and reduced levels of TNF-α, IL-6, resistin, MDA, GSH, CAT, Caspase-3, Caspase-9, Bax as well as Bax/Bcl-2 ratio in comparison to the lean- E. coli mice. Our results indicated that E. coli -induced pneumonia caused hepatic histopathological damage, increased hepatic apoptosis, oxidative damages, and higher levels of cytokines and adipocytokines. However, such changes showed less severely in the DIO mice than in the lean mice following E. coli pneumonia.

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