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[Research on olaquindox induced endoplasmic reticulum stress related apoptosis on nephrotoxicity]
Objective:
Renal tubular epithelial cell were exposed to olaquindox and detected the ROS and apoptosis related proteins, to investigate the renal tubular epithelial cell apoptosis through endoplasmic reticulum stress mediated pathway induced by olaquindox.
Methods:
MTT assay (1, 2, 3, 4, 5, 6, 7and 8 μmol/ml olaquindox exposure) was used to detect the effects of olaquindox on renal tubular epithelial cell proliferation to determine test concentrations. Hoechst-33258 was used to detect morphological changes on apoptotic cells in each group. Flow cytometry method was applied to detect the apoptosis rate and intracellular reactive oxygen, and western blot assay was performed to detect the levels of endoplasmic reticulum stress-related apoptosis proteins, GRP78, GRP94 and CHOP.
Results:
According to results of the MTT test, 1, 2, 3 and 4 μmol/ml olaquindox concentrations were determined for apoptosis analysis. With the increase of olaquindox concentration, apoptosis rate and levels of endoplasmic reticulum stress related apoptosis pathway protein GRP78, GRP94 and CHOP increased, levels of ROS were increased in every groups (P < 0.05) in 2 μmol/ml olaquindox groups and above. With the prolongation of olaquindox exposure, apoptosis rate and levels of endoplasmic reticulum stress related apoptosis pathway protein GRP78 and GRP94 increased in 12 and 24 h olaquindox exposure groups, whereas in groups of olaquindox exposed for 6, 12 and 24 h, levels of ROS and endoplasmic reticulum stress related apoptosis pathway protein CHOP increased (P < 0.05).
Conclusion:
Olaquindox can induce renal tubular epithelial cells to apoptosis and cause the renal toxicity, and the endoplasmic reticulum stress-related apoptosis maybe the associated toxicity pathway.
Insights
Olaquindox induces renal tubular epithelial cell apoptosis and toxicity. This occurs through endoplasmic reticulum stress, involving increased reactive oxygen species and specific protein levels.
Area of Science:
- Toxicology
- Cell Biology
- Biochemistry
Background:
- Renal tubular epithelial cells are crucial for kidney function.
- Olaquindox is an antimicrobial agent with potential toxic effects.
- Endoplasmic reticulum stress is implicated in various cellular dysfunctions.
Purpose of the Study:
- To investigate olaquindox-induced apoptosis in renal tubular epithelial cells.
- To explore the role of endoplasmic reticulum stress in olaquindox toxicity.
- To analyze the involvement of reactive oxygen species (ROS) and specific proteins in this pathway.
Main Methods:
- Cell proliferation assessed by MTT assay to determine olaquindox concentrations.
- Apoptotic cell morphology visualized using Hoechst-33258 staining.
- Apoptosis rate and intracellular ROS measured by flow cytometry.
- Western blot analysis for endoplasmic reticulum stress markers (GRP78, GRP94, CHOP).
Main Results:
- Olaquindox exposure increased apoptosis rate and ROS levels in a dose-dependent manner.
- Elevated levels of endoplasmic reticulum stress proteins (GRP78, GRP94, CHOP) were observed with increasing olaquindox concentration and exposure time.
- Significant increases in ROS and CHOP were noted at 2 μmol/ml olaquindox and above.
Conclusions:
- Olaquindox induces apoptosis and renal toxicity in renal tubular epithelial cells.
- Endoplasmic reticulum stress-mediated pathways are likely involved in olaquindox-induced renal toxicity.
- The study highlights a potential mechanism for olaquindox nephrotoxicity.
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