Chloramphenicol is a broad-spectrum antibiotic. (In Vitro):Chloramphenicol (1-100 μg/mL, 18-24 h) inhibits the HIF-1α pathway in NSCLC cells in a concentration-dependent manner.Chloramphenicol (100 μg/mL, 0-24 h) induces autophagy in NSCLC cells, substantially increases the levels of autophagic biomarkers (beclin-1, Atg12-Atg5 conjugates, and LC3-II).Chloramphenicol induces abnormal differentiation and inhibits apoptosis in activated T cells.Chloramphenicol can inhibit both bacterial and mitochondrial protein synthesis, causing mitochondrial stress and decreased ATP biosynthesis.chloramphenicol (1-100 μg/mL) can induce matrix metalloproteinase (MMP)-13 expression and increase MMP-13 protein.chloramphenicol (1-100 μg/mL) can activate c-Jun N-terminal kinases (JNK) and phosphatidylinositol 3-kinase (PI-3K)/Akt signaling, leading to c-Jun protein phosphorylation.Chloramphenicol acts primarily on the 50S subunit of bacterial 70S rihosomes and inhibits peptide bond formation by suppressing peptidyl transferase activity.(In Vivo):Chloramphenicol (0-3500 mg/kg, Gavage, daily, for 5 days) decreases erythrocytes and erythrocyte precursors and reduces marrow erythroid cells were at day 1 post-dosing, and returns to normal by 14 days post-dosing.
Chloramphenicol (0-3500 mg/kg, Gavage, daily, for 5 days) decreases erythrocytes and erythrocyte precursors and reduces marrow erythroid cells were at day 1 post-dosing, and returns to normal by 14 days post-dosing. Animal model: Female B6C3F1 mice (12-14 weeks old). Dosage: 0, 2500 and 3500 mg/kg. Administration: Gavage, daily, for 5 days. Result: Cessation of erythropoiesis was evident at day 1 post-dosing. A recovery was seen at day 7 post-dosing at the 2500 mg/kg dose level and at between 7 and 14 days at the 3500 mg/kg dose level. Myelotoxicity was most pronounced in the erythroid series at each dose level. Depressed femoral marrow BFU-E and CFU-E at day 1 post-dosing. All the blood and marrow parameters in the present study returned to normal by 14 days post-dosing.
In Vitro
Chloramphenicol (1-100 μg/mL, 18-24 h) inhibits the HIF-1α pathway in NSCLC cells in a concentration-dependent manner. Chloramphenicol (100 μg/mL, 0-24 h) induces autophagy in NSCLC cells, substantially increases the levels of autophagic biomarkers (beclin-1, Atg12-Atg5 conjugates, and LC3-II). Chloramphenicol induces abnormal differentiation and inhibits apoptosis in activated T cells. Chloramphenicol can inhibit both bacterial and mitochondrial protein synthesis, causing mitochondrial stress and decreased ATP biosynthesis. chloramphenicol (1-100 μg/mL) can induce matrix metalloproteinase (MMP)-13 expression and increase MMP-13 protein. chloramphenicol (1-100 μg/mL) can activate c-Jun N-terminal kinases (JNK) and phosphatidylinositol 3-kinase (PI-3K)/Akt signaling, leading to c-Jun protein phosphorylation. Chloramphenicol acts primarily on the 50S subunit of bacterial 70S rihosomes and inhibits peptide bond formation by suppressing peptidyl transferase activity. Cell Viability Assay Cell line: A549 and H1299 cells. Concentration: 0, 1, 10, 100 μg/mL. Incubation time: 3 h and 24 h. Result: In the 3-h-treated group, the viability of A549 and H1299 cells at 100 μg/mL concentration was 97.0 ± 3.9% and 98.1 ± 5.0%, respectively. The viability of A549 cells was 102.9 ± 1.3% and 99.2 ± 0.9%, whereas the viability of H1299 cells was 103.3 ± 1.9% and 93.8 ± 4.5%, under hypoxia and treatment with CoCl2, respectively. Western blot analysis. Cell line: A549 and H1299 cells. Concentration: 0, 1, 10, 50, 100 μg/mL. Incubation time: 18-24 h. Result: Inhibited HIF-1α protein accumulation in NSCLC cells in a concentration-dependent manner, while the expression levels of ARNT remained unaltered. Had no effect on CoCl2 (250 μM, 3 h treatment)-mediated HIF-1α protein accumulation and SENP-1 protein reduction. Western blot analysis. Cell line: A549 and H1299 cells. Concentration: 100 μg/mL. Incubation time: 0, 6, 12, 24 h. Result: Induced autophagy in NSCLC cells in a time-dependent manner. Upregulats the expression of beclin-1 and increased the levels of Atg12-Atg5 conjugates in both NSCLC cell lines, both in a time dependent and concentration-dependent manner. Augmented LC3-II and downregulated p62/STSQM1 in A549 cells. Induced an augmentation of p62/STSQM1, and a decrease in LC3-II levels in H1299 cells.
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