EXPERIMENTAL RESEARCH
C6orf120 gene deficiency may be vulnerable to carbon tetrachloride induced acute hepatic injury in rats
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Xin Li 1,2
 
 
 
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1
Department of Center of Integrated Traditional Chinese and Western Medicine, Peking University Ditan Teaching Hospital, Beijing, China
2
Department of Center of Integrated Traditional Chinese and Western Medicine, Beijing Ditan Hospital, Capital Medical University, Beijing, China
3
Department of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, China
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Department of Gastroenterology, Peking University Ditan Teaching Hospital, Beijing, China
Submission date: 2019-03-12
Final revision date: 2019-09-27
Acceptance date: 2019-10-14
Online publication date: 2020-02-24
 
Arch Med Sci 2022;18(6)
 
KEYWORDS
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ABSTRACT
Introduction:
The function of the C6orf120 gene, which encodes an N-glycosylated protein, remains unknown. The study was performed to characterize the utility of the C6orf120 gene in carbon tetrachloride-induced acute liver injury and to elucidate the potential underlying mechanisms by establishing a C6orf120 gene-knockout (C6orf120–/–) rat model.

Material and methods:
C6orf120-/- and wild-type (WT) rats were intraperitoneally administered with CCl4 (1 : 1 v/v in olive oil, 2 µl/g). Rats were sacrificed 24 h after CCl4 administration. Liver tissues were collected for H&E, IHC, qRT-PCR, and Western blot analysis.

Results:
C6orf120 gene deficiency may be vulnerable to CCl4-induced acute liver injury in rats as indicated by the high levels of alanine aminotransferase (WT: 388.7 ±55.96 vs. C6orf120–/–: 915.9 ±118.8, p < 0.001) and greater degree of pathological damage. Quantitative reverse transcription polymerase chain reaction showed that the mRNA levels of inflammation-associated cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-, in liver tissues were increased in C6orf120–/– rats compared with those in WT rats. Moreover, western blot showed that the protein expression of cytokines nucleotide-binding oligomerization domain leucine rich repeat and pyrin domain containing 3 (NLRP3), caspase-1, IL-1β, nuclear factor-κB, c-Jun N-terminal kinases, and Bax were increased in C6orf120–/– rats compared with those in WT rats.

Conclusions:
C6orf120–/– rats were susceptible to CCl4-induced liver injury, which may be related to NLRP3 inflammasome and JNK signaling pathway activation.

eISSN:1896-9151
ISSN:1734-1922