TABLE 2.
Summarization of the effects of drugs acting on PPARγ in hepatic IRI.
| Drugs act on PPARγ | IRI models | Main effects | Conclusion | Reference |
|---|---|---|---|---|
| 15 daysPGJ2 a | Balb/c mice (7 weeks, 22 ± 2 g) | Decreased serum TNF-α, IL-1β, F4/80, beclin-1, LC3, apoptotic cells, and autophagosomes. Upregulated Bcl-2/Bax ratio | 15 days-PGJ2 protects liver IR injury via reducing Kupffer cell activation and activating the Nrf2 pathway | Chen K. et al. (2017) |
| 15 days-PGJ2 a | Balb/c mice (7 weeks, 22 ± 2 g) | Reduced serum TNF-a, IL-1b and ROS, inhibited apoptosis, and autophagic cell death | 15 days-PGJ2 alleviates liver injury by up-regulating HO-1 and inhibiting hepatic cell autophagy | Chen et al. (2016) |
| Dexmedetomidine b | C57BL/6 mice (8 weeks) | Inhibited intrahepatic pro-inflammatory innate immune activation | Dexmedetomidine attenuates liver IRI via PPARγ/STAT3 pathway | Zhou et al. (2020) |
| Losartan b | C57BL/6 mice (8–10 weeks) | Reduced ALT activity, TNF-α and IL-6 levels, decreased in apoptosis | Losartan ameliorates liver IRI with PPARγ involvement, and inhibits RAGE-mediated signaling pathway | Koh et al. (2013) |
| Pioglitazone c | Wistar rats (200–250 g) | Reduced TNF-α, MDA, NADPH oxidase mRNA, apoptotic cell death, and oxidative stress, and increased Nrf2, PPARγ1, Hmox1, and TRx expression | PPARγ is a potential target to protect liver in patients with renal IRI | Elshazly and Soliman. (2019) |
| Rosiglitazone c | C57BL/6 (10–12 weeks) | Reduced apoptosis, necrosis, nitric oxide + Kupffer cell population, and increased CD206 + Kupffer cell population | PPARγ can be an essential tool to ameliorate liver outcomes by reducing the pro-inflammatory phenotype of KCs and IRI | Linares et al. (2018) |
Nrf2, nuclear factor erythroid-related factor 2; RAGE, receptor for advanced glycation end product; MDA, malondialdehyde; Hmox1, hepatic hemoxygenase-1; TRx, hepatic thioredoxin.
a
PPARγ natural ligand.
b
PPARγ agonist.
c
PPARγ synthetic ligand.