Abstract
Objective: Sitagliptin (Sitagtin) is widely involved in the treating process for several diseases in humans, covering DN (Diabetic Nephropathy). In the present research, the aim was at examining the roles of the miR-425-5p/TGFβ /P65 pathway in a DN rat model treated by Sitagtin. Methods: The subjects fed high-fat food were killed. Besides, new kidney specimens were placed in formaldehyde solution for histopathology-based observing process. Subsequently, Coomassie brilliant blue approach was used to determine urine protein excretion for 24 hours. Lastly, by bicinchoninic acid protein assay, proteins harvested from kidney tissue were detected. Results: Firstly, it was identified that miR-425-5p showed the highest expression in Sitagtin treatment cells compared to PBS treatment through miRNA microarray analysis. In addition, Sitagtin suppressed the HBZY-1 cell lines' proliferation, which may inhibit TGFβ /P65 expression through upregulating miR-425-5p. Furthermore, after HBZY-1 cells induced by high glucose (HG) were administrated with Sitagtin, miR-425-5p and si TGF /P65 inhibited HBZY-1 cells from proliferating. It was proved that TGFβ /P65 was one of the targeted genes of miR-425-5p. Lastly, TGFβ /P65 expression was decreased in the DN administrated with Sitagtin; the 24 h urinary protein excretion was decreased in Sitagtin-administrated DN rats. Conclusion: The study demonstrated that Sitagtin inhibited HBZY 1 cells through miR-4255p/TGFβ /P65 signaling.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
