Bazhen Decoction Protects against Acetaminophen Induced Acute Liver Injury by Inhibiting Oxidative Stress, Inflammation and Apoptosis in Mice

Abstract

Bazhen decoction is a widely used traditional Chinese medicinal decoction, but the scientific validation of its therapeutic potential is lacking. The objective of this study was to investigate corresponding anti-oxidative, anti-inflammatory and anti-apoptosis activities of Bazhen decoction, using acetaminophen-treated mice as a model system. A total of 48 mice were divided into four groups. Group I, negative control, treated with vehicle only. Group II, fed with 500 mg/kg/day Bazhen decoction for 10 continuous days. Group III, received a single dose of 900 mg/kg acetaminophen. Group IV, fed with 500 mg/kg/day Bazhen decoction for 10 continuous days and a single dose of 900 mg/kg acetaminophen 30 min before last Bazhen decoction administration. Bazhen decoction administration significantly decrease acetaminophen-induced serum ALT, AST, ALP, LDH, TNF-α, IL-1β, ROS, TBARS and protein carbonyl group levels, as well as GSH depletion and loss of MMP. Bazhen decoction restore SOD, CAT, GR and GPx activities and depress the expression of pro-inflammatory factors, such as iNOS, COX-2, TNF-α, NF-κB, IL-1β and IL-6, respectively. Moreover, Bazhen decoction down-regulate acetaminophen-induced Bax/Bcl-2 ratio, caspase 3, caspase 8 and caspase 9. These results suggest the anti-oxidative, anti-inflammatory and anti-apoptosis properties of Bazhen decoction towards acetaminophen-induced liver injury in mice.

Quercetin prevents alcohol‑induced liver injury through targeting of PI3K/Akt/nuclear factor‑κB and STAT3 signaling pathway

“…Bcl-2 protein can also promote the synthesis of GSH and inhibit the consumption of mitochondria GSH, to play an antioxidant role, in order to maintain mitochondrial redox homeostasis. It is also found that the lower expression level of Bcl-2 means the higher level of lipid peroxidation (30). Caspase-3 is an important executive molecule in the process of apoptosis (9).…”

“…Bax/Bcl-2 ratio can also reflect the degree of apoptosis to some extent (30). Bcl-2 protein can also promote the synthesis of GSH and inhibit the consumption of mitochondria GSH, to play an antioxidant role, in order to maintain mitochondrial redox homeostasis.…”

Translational Implications of the Alcohol-Metabolizing Enzymes, Including Cytochrome P450-2E1, in Alcoholic and Nonalcoholic Liver Disease

“…In fact, JNK-null mice or iNOSnull mice were resistant to alcohol-or HFD-induced insulin resistance and apoptosis. Specific deletion or suppression of JNK1 or iNOS, with either using a specific siRNA or an inhibitor, or in knockout mouse strain, can also lead to resistance to HFD-induced insulin resistance and hepatocytes death or drug-induced liver injury (DILI) (Charbonneau & Marette, 2010;Fujimoto et al, 2005;He et al, 2015;Kamanaka et al, 2003;Saberi et al, 2014;Seki et al, 2012;Singh et al, 2009;Song, Fu, Xia, Su, & Song, 2014;Tipoe et al, 2006;. The opposite case with overexpression of these pro-oxidant proteins would increase the tissue sensitivity toward apoptotic death.…”

Radiation Induced Gastrointestinal Damage and Protection: Nigella Sativa Seed Extract and Thymoquinone

“…These may include the prevention of the pathways involved in oxidative stress, inflammation, apoptosis and gastric acid production 43,44 . Whole body exposing to acute doses of gamma irradiation either (6 Gy), were found to exert an oxidative stress due to generation of ROS, which characterised by elevation in TBARS and nitrite contents and depletion in reduced glutathione, as well as elevation in MPO activity and enhancing the production of cytokines such as TNF-α 45 , an effect which could have been due to ROS-mediated activation of the transcription factor Nf-κB [46][47] . Pretreatment of NS seed extract and TQ protect the tissues from oxidative stress induced by irradiation through protection against elevation in TBARS.…”