TABLE 3.
Pharmacological activities of celastrol in the treatment of liver injury.
| Model style | Cell/animal | Inducer | Dosage of celastrol | Treatment time | Phenotype/mechanism | Reference |
|---|---|---|---|---|---|---|
| Chemicals induced liver injury | HepG2 cells | APAP | 50, 100, and 200 nM | 24 h | Ameliorated oxidative stress and cytotoxicity caused by APAP | Jannuzzi et al. (2018) |
| Chemicals induced liver injury | Male BALB/c mice | APAP | 2 mg/kg by i.p injection | 2 h prior APAP-induction | Prevented oxidative stress and inflammation by attenuating inflammatory cells accumulation and reducing inflammation factors | Abdelaziz et al. (2017) |
| Chemicals induced liver injury | Male WT mice and Ppara−/− mice on the 129/Sv genetic background | CCl4 | 10 mg/kg by oral treatment | 5 days | Inhibited inflammatory cytokine and oxidative stress by suppressing PPARα signaling pathway, the effects of celastrol attenuated DCA-EGR1-inflammatory factor signaling in CCl4-induced PPARα deleted mice | Zhao et al. (2020) |
| Chemicals induced liver injury | Male Sprague | CCl4 | 0.25 mg/kg/day,0.5 mg/kg/day,1 mg/kg/day by i.p injection | 4 weeks | Suppressed inflammation in liver fibrosis by activating AMPK-SIRT3 signaling | Wang et al. (2020) |
| Dawley rats | ||||||
| Cholestatic liver injury | Male C57BL/6J mice | ANIT | 10 mg/kg/day by oral administration | 5 days | Alleviated cholestatic liver injury by activation SIRT1-FXR signaling pathway | Zhao et al. (2019b) |
| Male C57BL/6J mice and Fxr-null mice | TAA | FXR disruption attenuated protection effects of celastrol on cholestatic liver injury | ||||
| Cholestatic liver injury | Female Sprague-Dawley rats | EE | 5 mg/kg/day by an oral administration | 5 days | Alleviated phenotype of ICP by inhibited MMP-2 and MMP-9 | Guo et al. (2019) |
| Sepsis induced liver injury | Male Sprague Dawley rats | CLP | 1 mg/kg by i.p injection | 60 min before CLP | Attenuated inflammation by suppressing NF- κB, reduced TLR-4 and 5-LOX expression, downregulated the expression of IL-6 | El-Tanbouly et al. (2017) |
| Sepsis induced liver injury | Male C57BL/6 mice | LPS | 1.5 mg/kg/day by i.p injection | 24 h before LPS induction, after LPS intoxiant for another 24 h | Aggravated liver injury through activating inflammation and deteriorating oxidative stress | Wu et al. (2018) |
| Sepsis induced liver injury | Male C57BL/6J mice and NLRP3-/- mice | P. acnes/LPS | 0.5 or 0.25 mg/kg by i.p injection on every other day after P. acnes induction for 3 days | 3 days | Suppressed NLRP3 inflammasome formation by blocking deubiquitylation of NLRP3 | Yan et al. (2021) |
APAP, acetaminophen; CCl4, carbon tetrachloride; AMPK, Adenosine 5′-monophosphate (AMP)-activated protein kinase; SIRT3, sirtuin3; PPARα, Peroxisome Proliferator Activated Receptor α; DCA, deoxycholic acid; EGR1, Early Growth Response 1; ANIT,α-naphthyl isothio-cyanate; TAA, thioacetamide; SIRT1, sirtuin1; FXR, Farnesoid X receptor; EE, 17 -ethinyl estradiol; ICP, intrahepatic cholestasis of pregnancy; MMP-2, Matrix metalloproteinase-2; MMP-9, Matrixmetalloproteinase-9; CLP, cecal ligation and puncture; NF-κB, nuclear factor kappa-B; TLR4, Toll-like receptor 4; 5-LOX, 5-Lipoxygenase; IL-6, Interleukin-6; LPS, lipopolysaccharides; P. acnes/LPS, Propionibacterium acnes/lipopolysaccharides; NLRP3, NOD-like receptor protein 3.