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Tigecycline attenuates apoptosis and the release of pro‐inflammatory cytokines in Lipopolysaccharide‐treated PC12 cells
Author(s) -
Yagnik Radhi M,
Benzeroual Kenza E.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1004.10
Subject(s) - tigecycline , neuroinflammation , minocycline , lipopolysaccharide , pharmacology , apoptosis , tumor necrosis factor alpha , microglia , caspase 3 , medicine , inflammation , chemistry , immunology , microbiology and biotechnology , programmed cell death , biology , antibiotics , biochemistry
Several inflammatory cytokines such as TNF‐alpha, and IL‐1beta have been involved in the neuroinflammation associated with Alzheimer's disease (AD). Tigecycline, a glycylcycline antibiotic and an analog of Minocycline, is shown to exert anti‐inflammatory effects that are distinct from its anti‐microbial activity. In this study, the inhibitory effects of tigecycline on TNF‐alpha and IL‐1beta release in lipopolysaccharide (LPS) treated PC12 (a neuronal cell line) cells were examined using Western blot and ELISA, respectively. Further, the effect of tigecycline on nitric oxide (NO) release was also evaluated. To determine the involvement of apoptotic machinery, cellular caspase‐3 levels as well as the pro‐apoptotic Bad levels were measured. The results showed that tigecycline significantly attenuated the levels of TNF‐alpha and IL‐1beta, as well as NO levels in LPS‐treated PC12 cells. The caspase assay revealed a significant decrease in the caspase‐3 levels in the drug treated cells. The results of pro‐apoptotic Bad levels showed a protective mechanism of the drug. The findings of our study suggest that tigecycline may be considered as a potential therapeutic agent in the neuroinflammation associated with AD or other neurodegenerative disorders.