|
Chronic kidney disease (CKD) is a worldwide public health problem, resulting in a significant burden on the health system. PBM is effective in mitigating inflammation, mitochondrial dysfunction, and oxidative stress, all of which are factors inherent in CKD. The aim of this study was to identify the direct effects of PBM in an in-vitro model of CKD. In vitro human proximal tubular cells (HK2 cells) were pre-treated with low (1.38 J/cm2) or high dosage (2.75J/cm2) of PBM. Cells were then incubated with TGF-β1 (2 ng/ml) for 48 hours with or without PBM irradiation every 24 hours. The SHAM groups were processed under the exact same conditions except in the absence of PBM irradiation. The expression levels of inflammatory markers monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), fibrotic marker fibronectin (FN), antioxidative markers superoxide dismutase 1 (SOD1) and SOD2 were measured by qRT-PCR or ELISA The results showed that TGF-β1 significantly increased MCP-1, TNF-α, and fibronectin mRNA expression in HK2 cells, which was significantly reversed by the low dosage of PBM (0.45 J/cm2, P<0.05), but not the higher dosage of PBM (0,9 J/cm2) when compared with the SHAM control group. The dose-response characteristics of PBM observed in this study followed the biphasic pattern. In conclusion, the present study suggests that PBM directly reduced inflammation and fibrosis in kidney tubular cells when used at the appropriate dose.
|
