Table 4 Drugs targeting sepsis and complications by down-regulation of HIF-1α
Drug Names | The role of HIF-1α | Modulation of HIF-1α | Model | References |
|---|---|---|---|---|
Lidocaine | Inhibiting glycolysis to attenuate inflammatory response | Down (indirectly through NF-κB pathway) | LPS-induced sepsis mouse | [115] |
HCP | Reduce intestinal damage in H1N1 virus-infected individuals | Down (indirectly through TLR4 pathway) | H1N1 virus infected mouse mice | [116] |
XJDHT | Participation in aerobic glycolysis in sepsis | Down (indirectly through TLR4 pathway) | CLP-induced sepsis rats | [117] |
Cynaroside | Attenuates liver injury | Down (indirectly through PKM2 pathway) | CLP-induced sepsis mouse | [118] |
Norisoboldine | Mitigates sepsis-induced acute lung injury | Down (indirectly through PKM2 pathway) | LPS-induced sepsis mouse | [119] |
LBP | Altering glycolysis and the M1 differentiation of macrophages | Down (indirectly through PKM2 pathway) | LPS-induced macrophages model | [120] |
Cya | Affects B cell Migration | Down (stimulate PHD activity) | Human and mouse B cell | [121] |
AV | Promoting inflammatory responses | Down (stimulate PHD2 activity) | CLP-induced sepsis mouse | [122] |
TIIA | Promoting inflammatory responses | Down (indirectly through PI3K and MAPK pathway) | LPS-induced lung injury mouse | [123] |
Propofol | Promoting inflammatory responses | Down (indirectly through MAPK pathway) | Mouse model of endotoxemia | [124] |
Resveratrol | Improvement of vasodilatory function in a septic shock model | Down (not given) | CLP-induced septic shock rats | [125] |
Chicoric acid | Mediated glycolysis and mitochondrial oxidative burst | Down (reducing ROS production) | LPS-induced sepsis mouse | [126] |
TASE | Leading to endotoxin tolerance in sepsis monocytes | Down (indirectly through IRAK-M pathway) | Monocytes in patients with sepsis | [127] |
AmB | Regulation of EPO expression | Down (reinforcing FIH-mediated repression) | Hypoxia and anemia rats | [128] |
Rosmarinic acid | Regulation of LPS-induced microglial M1 polarization | Down (indirectly through RACK1 pathway) | CLP-induced sepsis mouse | [129] |
2ME2 | Promoting inflammatory responses | Down (reduced HIF-1α activity) | CLP- and LPS-induced sepsis mouse | [130] |
Emodin | Modulates intestinal barrier injury | Down (inhibits the expression of HIF-1α) | LPS-induced intestinal epithelial cells model | [131] |
N5P | Promoting inflammatory responses | Down (inhibits the expression of HIF-1α) | ALI rat model | [132] |
Valproic acid | Participation in burn-induced gut barrier dysfunction | Down (inhibits HIF-1α accumulation) | Rat burn model | [133] |
DHMF | Promoting inflammatory responses | Down (inhibits HIF-1α accumulation) | LPS-induced lung injury mouse | [134] |
Eriocitrin | Regulation of glycolysis in sepsis | Down (inhibition of HIF-1α mRNA) | LPS-induced sepsis-associated ALI mouse | [135] |
Metformin | Promoting inflammatory responses | Down (inhibition of HIF-1α mRNA) | LPS-induced sepsis-associated liver injury mouse | [136] |
Landiolol | Involved in sepsis-related AKI | Down (inhibition of HIF-1α mRNA) | Mouse model of endotoxaemia | [137] |
Enoxaparin | Causes diaphragm damage | Down (inhibition of HIF-1α mRNA and Protein) | LPS-induced sepsis mouse | [138] |
Dexmedetomidine | Participation in aerobic glycolysis in sepsis | Down (inhibition of HIF-1α mRNA and Protein) | LPS-treated macrophages | [139] |