Effect of Lactobacillus reuteri GMNL-263 treatment on renal fibrosis in diabetic rats.
Hyperglycemia is the most important factor in the progression of renal fibrosis in diabetic kidney. Prevention and treatment of renal fibrosis may improve diabetic nephropathy. To explore whether probiotic Lactobacillus reuteri GMNL-263 treatment was linked to altered hyperglycemia-mediated renal fibrosis in diabetic kidney, the mechanisms of L. reuteri GMNL-263 treatment responsible for the inhibition of renal fibrosis in streptozotocin (STZ)-induced diabetic rats were examined. Diabetic rats were induced by intraperitoneal injection of STZ (50 mg/kg). Induction of diabetes was confirmed by measurement of the blood glucose using the glucose oxidase method, and hyperglycemic rats with levels >16 mmol/L were used. We found that L. reuteri GMNL-263 treatment caused reduction of glycated hemoglobin and blood glucose levels in STZ-induced diabetic rats for 28 days (all p<0.05). Treatment with L. reuteri GMNL-263 increased body weight but decreased kidney weight in diabetic rats as compared to diabetic control (p<0.05). In diabetic renal cortex, the Janus kinase 2/signal transducers and activators of transcription 1 (but not extracellular signal-regulated kinase/c-Jun N-terminal kinase/p38 mitogen-activated protein kinase) activation was markedly blocked by L. reuteri GMNL-263 treatment. The ability of L. reuteri GMNL-263 treatment to inhibit renal fibrosis was verified by the observation that it significantly decreased protein levels of plasminogen activator inhibitor-1, p21(Waf1/Cip1), α-smooth muscle actin, and fibronectin in diabetic renal cortex. The results obtained in this study indicate that L. reuteri GMNL-263 treatment may protect STZ-induced diabetic rats from hyperglycemia-enhanced renal fibrosis.
Lu
Ying-Chen
YC
Department of Biological Science and Technology, Chung Hwa University of Medical Technology, Tainan 717, Taiwan, ROC.
Yin
Li-Te
LT
Chang
Wen-Teng
WT
Huang
Jau-Shyang
JS
D000199:Actins / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D003928:Diabetic Nephropathies / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D005353:Fibronectins / Q000378:metabolism; D005355:Fibrosis; D006442:Glycated Hemoglobin / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D053614:Janus Kinase 2 / Q000378:metabolism; D007668:Kidney / Q000473:pathology; D007672:Kidney Cortex / Q000201:enzymology / Q000378:metabolism; D052200:Limosilactobacillus reuteri; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D019936:Probiotics; D051381:Rats; D017207:Rats, Sprague-Dawley; D050791:STAT Transcription Factors / Q000378:metabolism
D000199:Actins; D001786:Blood Glucose; D005353:Fibronectins; D006442:Glycated Hemoglobin; D048031:JNK Mitogen-Activated Protein Kinases; D053614:Janus Kinase 2; D020928:Mitogen-Activated Protein Kinases; D017395:Plasminogen Activator Inhibitor 1; D050791:STAT Transcription Factors