Curcumin and Selenium Prevent Lipopolysaccharide/Diclofenac-Induced Liver Injury by Suppressing Inflammation and Oxidative Stress.
Manal H Al-DossariLaila M FaddaHala A AttiaIman H HasanAyman Moawad MahmoudPublished in: Biological trace element research (2019)
Diclofenac (DCL), an anti-inflammatory drug used to reduce pain and inflammation, ranks in the top causes of drug-induced liver injury. The inflammatory stress induced by inflammagens is implicated in DCL-induced liver injury. Curcumin (CUR) and selenium (Se) possess anti-inflammatory effects; therefore, this study evaluated their protective potential against lipopolysaccharide (LPS)/DCL-induced liver injury. Rats received CUR and/or Se for 7 days followed by a single intravenous administration of LPS 2 h before a single injection of DCL and two other doses of CUR and/or Se 2 and 8 h after DCL. Administration of nontoxic doses of LPS and DCL resulted in liver damage evidenced by the significantly elevated liver function markers in serum. LPS/DCL-induced liver injury was confirmed by histological alterations, increased lipid peroxidation and nitric oxide, and diminished glutathione and superoxide dismutase. CUR and/or Se prevented liver injury, histological alterations, and oxidative stress and boosted antioxidant defenses in LPS/DCL-induced rats. In addition, CUR and/or Se reduced serum C-reactive protein, liver pro-inflammatory cytokines, and the expression of TLR4, NF-κB, JNK, and p38, and upregulated heme oxygenase-1 (HO-1). In conclusion, CUR and/or Se mitigated LPS/DCL-induced liver injury in rats by suppressing TLR4 signaling, inflammation, and oxidative stress and boosting HO-1 and other antioxidants. Therefore, CUR and Se can hinder the progression and severity of liver injury during acute inflammatory episodes.
Keyphrases
- oxidative stress
- drug induced
- liver injury
- anti inflammatory
- inflammatory response
- diabetic rats
- lps induced
- toll like receptor
- induced apoptosis
- dna damage
- ischemia reperfusion injury
- nitric oxide
- adverse drug
- emergency department
- immune response
- chronic pain
- pi k akt
- hydrogen peroxide
- intensive care unit
- ultrasound guided
- nuclear factor
- cell proliferation
- heat shock
- pain management
- hepatitis b virus
- binding protein
- risk assessment
- fatty acid