Aims: microRNAs (miRNAs) occupy a vital position in diseases. This research aims to detect miR-103 influence on LPS-resulted HK-2 cells inflammation damage. Methods: Cells were exposed to LPS for inducing injury. CCK-8 and flow cytometry were introduced to detect cell viability and apoptosis rate, respectively. ELISA, qRT-PCR and western blot were respectively used to explore inflammation factors production and relative proteins expression. The relationship between miR-103 and c-Myc was analysed through luciferase reporter assay. Results: LPS led to significant inhibition of cell viability (p < .05) and proliferation-related proteins expression. It also increased the apoptosis rate (p < .05) and promoted inflammation cytokines overproduction (p < .001). Besides, miR-103 was elevated by LPS (p < .01), and aggravated LPS-induced damage above, while miR-103 inhibitor attenuated this impairment (p < .05, p < .01 or p < .001). However, c-Myc silence abolished miR-103 inhibitor protective effect on cell proliferation (p < .05), apoptosis (p < .01) and inflammation factors expression (p < .05 or p < .01), representing a negative relationship between them. Besides, the activity of NF-κB as well as JAK/STAT pathways was controlled by miR-103, also, mediated through c-Myc. Conclusions: miR-103 mimic enhanced LPS-caused inflammation damage by silencing c-Myc in HK-2 cell line.
Aims: microRNAs (miRNAs) occupy a vital position in diseases. This research aims to detect miR-103 influence on LPS-resulted HK-2 cells inflammation damage. Methods: Cells were exposed to LPS for inducing injury. CCK-8 and flow cytometry were introduced to detect cell viability and apoptosis rate, respectively. ELISA, qRT-PCR and western blot were respectively used to explore inflammation factors production and relative proteins expression. The relationship between miR-103 and c-Myc was analysed through luciferase reporter assay. Results:LPS led to significant inhibition of cell viability (p < .05) and proliferation-related proteins expression. It also increased the apoptosis rate (p < .05) and promoted inflammation cytokines overproduction (p < .001). Besides, miR-103 was elevated by LPS (p < .01), and aggravated LPS-induced damage above, while miR-103 inhibitor attenuated this impairment (p < .05, p < .01 or p < .001). However, c-Myc silence abolished miR-103 inhibitor protective effect on cell proliferation (p < .05), apoptosis (p < .01) and inflammation factors expression (p < .05 or p < .01), representing a negative relationship between them. Besides, the activity of NF-κB as well as JAK/STAT pathways was controlled by miR-103, also, mediated through c-Myc. Conclusions: miR-103 mimic enhanced LPS-caused inflammation damage by silencing c-Myc in HK-2 cell line.