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Abstract: SA-PO419

Photobiomodulation Protects High-Fat Diet-Induced Diabetic Kidney Injury via Inhibition of Inflammation

Session Information

Category: Diabetic Kidney Disease

  • 701 Diabetic Kidney Disease: Basic

Authors

  • Bian, Ji, Kolling Institute, Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales, Australia
  • Bicknell, Brian, College of Health and Medicine, Australian National University, Canberra, Australian Capital Territory, Australia
  • Liebert, Ann, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia
  • Chen, Xinming, Kolling Institute, Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales, Australia
  • Huang, Chunling, Kolling Institute, Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales, Australia
  • Pollock, Carol A., Kolling Institute, Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales, Australia

Group or Team Name

  • Renal Group.
Background

Innovative therapeutic strategies for DKD are urgently needed due to limitations of current treatments. PBM, using red or near-infrared light to modulate cellular function, has gained increasing interest among available therapeutic strategies for many diseases due to its wide variety of positive effects, such as suppressing inflammation, improving mitochondrial activity, and alleviating oxidative stress, which are all inherent in DKD. However, the potential role of PBM in treating DKD has not yet been explored.

Methods

In vitro, human proximal tubular cells (HK2 cells) pre-treated with low dose (4.32 J) or high dose (8.64J) PBM were then incubated with TGF-β1 (2 ng/ml) for 48 hours with or without PBM irradiation every 24h. In vivo, high-fat diet (HFD)-induced DKD mice were treated with low dose (7.2J) or high dose (18J) PBM 3 times per week commencing at 12 weeks of HFD and continue for 12 weeks. SHAM treatment was identical but with laser diodes switched off. Renal function, fibrotic and inflammatory markers were examined.

Results

In vitro results showed that TGF-β1 induced overexpression of fibronectin and tumour necrosis factor (TNF-α) ((P<0.01) at both mRNA and protein levels, which were significantly reversed by low (P<0.05) but not high PBM dose. Moreover, low but not high PBM dose significantly inhibited TGF-β 1-induced phosphorylation of p65 in comparison with the SHAM group. In vivo, low but not high PBM dose improved HFD-induced kidney injury with significant decreases in the levels of blood urea nitrogen, 24h albumin, and urine albumin-creatinine ratio (P<0.05). Furthermore, HFD-induced overexpression of collagen IV, TNF-α, a-SMA, TGF-β1, F4/80, and CD68 were reversed by low (P<0.05) but not high dose of PBM.

Conclusion

PBM exerts its reno-protective effect via inhibiting inflammation in in vitro and in high-fat diet-induced diabetic mice. This effect is biphasic, with PBM above the therapeutic dose showing no improvement in renal function.

Funding

  • Government Support – Non-U.S.