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Breviscapine ameliorates CCl4?induced liver injury in mice through inhibiting
inflammatory apoptotic response and ROS generation
#MMPMID29717768
Liu Y
; Wen PH
; Zhang XX
; Dai Y
; He Q
Int J Mol Med
2018[Aug]; 42
(2
): 755-768
PMID29717768
show ga
Acute liver injury is characterized by fibrosis, inflammation and apoptosis,
leading to liver failure, cirrhosis or cancer and affecting the clinical outcome
in the long term. However, no effective therapeutic strategy is currently
available. Breviscapine, a mixture of flavonoid glycosides, has been reported to
have multiple biological functions. The present study aimed to investigate the
effects of breviscapine on acute liver injury induced by CCl4 in mice. C57BL/6
mice were subjected to intraperitoneal injection with CCl4 for 8 weeks with or
without breviscapine (15 or 30 mg/kg). Mice treated with CCl4 developed acute
liver injury, as evidenced by histological analysis, Masson trichrome and Sirius
Red staining, accompanied with elevated levels of alanine aminotransferase and
aspartate aminotransferase. Furthermore, increases in pro?inflammatory cytokines,
chemokines and apoptotic factors, including caspase?3 and poly(ADP ribose)
polymerase?2 (PARP?2), were observed. Breviscapine treatment significantly and
dose?dependently reduced collagen deposition and the fibrotic area. Inflammatory
cytokines were downregulated by breviscapine through inactivating Toll?like
receptor 4/nuclear factor-?B signaling pathways. In addition, co?administration
of breviscapine with CCl4 decreased the apoptotic response by enhancing B?cell
lymphoma-2 (Bcl?2) levels, while reducing Bcl?2?associated X protein, apoptotic
protease activating factor 1, caspase?3 and PARP activity. Furthermore,
CCl4?induced oxidative stress was blocked by breviscapine through improving
anti?oxidants and impeding mitogen?activated protein kinase pathways. The present
study highlighted that breviscapine exhibited liver?protective effects against
acute hepatic injury induced by CCl4 via suppressing inflammation and apoptosis.
|*Carbon Tetrachloride
[MESH]
|Animals
[MESH]
|Anti-Inflammatory Agents/*therapeutic use
[MESH]
|Antioxidants/*therapeutic use
[MESH]
|Apoptosis/*drug effects
[MESH]
|Cell Line
[MESH]
|Chemical and Drug Induced Liver Injury/*drug therapy/immunology/pathology
[MESH]
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