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| Study on the repairment mechanism of berberine on podocyte injury induced by high glucose based on JAK2-STAT3 pathway |
| Hits 1029 Download times 687 Received:June 16, 2020 |
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| DOI
10.11656/j.issn.1672-1519.2020.09.25 |
| Key Words
diabetic nephropathy;podocytes;berberine;JAK2;STAT3 |
| Author Name | Affiliation | | GUO Xiaolei | Emergency Department, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China |
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| Abstract
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| [Objective] The mechanism of berberine on the repair of podocyte injury induced by high glucose was investigated from JAK2-STAT3 pathway.[Methods] MPC-5 immortalized mouse podocytes were cultured and divided into normal glucose concentration group (5 mmol/L glucose),high glucose concentration group (30 mmol/L glucose),high glucose + 10 μmol/L berberine Group,high glucose + 25 μmol/L berberine group and high sugar + 50 μmol/L berberine group. The normal sugar concentration group was routinely cultured;the other groups were cultured for 48 h in the corresponding medium. Cell viability was detected by MTT assay;cell migration ability was detected by transwell assay;podocyte barrier function was measured by albumin flow rate assay;JAK2 and STAT3 mRNA and protein expression were detected by RT-PCR and Western Blot assay,respectively.[Results] Compared with the normal glucose concentration group,the survival rate of podocytes was significantly decreased after high glucose stimulation,the migration ability was increased,the barrier function was decreased,and the mRNA and protein expression levels of JAK2 and STAT3 were increased (all P<0.01). It promoted the survival of podocytes,decreased the migration ability,increased the barrier function,and decreased the expression of JAK2 and STAT3 mRNA and protein and the concentration was dependently (P<0.05,P<0.01).[Conclusion] Berberine can protect podocyte injury induced by high glucose,improve the survival rate of podocytes in high glucose environment,reduce its migration rate and maintain its barrier function. The mechanism may be related to the regulation of JAK2 and STAT3 gene and protein expression. |
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