Protective effect of yacon leaves extract (Smallanthus sonchifolius (Poepp.) H. Rob) through antifibrosis, anti-inflammatory, and antioxidant mechanisms toward diabetic nephropathy.

Background and purpose: Diabetic nephropathy (DN) is a chronic kidney failure, which may lead to fatality. Mesangial cell proliferation, renal inflammation, stress oxidative, and fibrosis are involved in DN progression. Yacon leaves (Smallanthus sonchifolius (Poepp.) H. Rob.) contains large amounts of phenolic compounds and it has the ability to inhibit oxidative stress, inflammation, and fibrosis. Considering the potential of yacon leaves extract (YLE), it may be used for DN treatment. This research aimed to elucidate YLE's potential as anti-DN through anti-inflammatory, antioxidant, and antifibrosis mechanisms. Experimental approach: Mesangial cells were induced by glucose 20 mM for 5 days and treated with YLE concentrations as much as 5, 10, and 50 µg/mL. TGF-ß1, TNF-α, and MDA levels were measured using the ELISA method. SMAD2, SMAD3, SMAD4, and SMAD7 gene expressions were analyzed using the qRT-PCR method. Findings/Results: YLE at 5, 10, and 50 µg/mL could reduce the levels of TGF-ß1, TNF-α, and MDA compared with the DN cells model. YLE could reduce gene expressions of SMAD2, SMAD3, and SMAD4 and increase SMAD7 expression. Conclusion and implications: YLE potentially mitigated diabetic nephropathy through antifibrosis, anti-inflammatory, and antioxidant capacities.

Quercetin prevents chronic kidney disease on mesangial cells model by regulating inflammation, oxidative stress, and TGF-ß1/SMADs pathway.

Background: Chronic kidney disease (CKD) happens due to decreasing kidney function. Inflammation and oxidative stress have been shown to result in the progression of CKD. Quercetin is widely known to have various bioactivities including antioxidant, anticancer, and anti-inflammatory activities. Objective: To evaluate the activity of quercetin to inhibit inflammation, stress oxidative, and fibrosis on CKD cells model (mouse mesangial cells induced by glucose). Methods and Material: The SV40 MES 13 cells were plated in a 6-well plate with cell density at 5,000 cells/well. The medium had been substituted for 3 days with a glucose-induced medium with a concentration of 20 mM. Quercetin was added with 50, 10, and 5 µg/mL concentrations. The negative control was the untreated cell. The levels of TGF-ß1, TNF-α, and MDA were determined using ELISA KIT. The gene expressions of the SMAD7, SMAD3, SMAD2, and SMAD4 were analyzed using qRT-PCR. Results: Glucose can lead to an increase in inflammatory cytokines TNF-α, TGF-ß1, MDA as well as the expressions of the SMAD2, SMAD3, SMAD4, and a decrease in SMAD7. Quercetin caused the reduction of TNF-α, TGF-ß1, MDA as well as the expression of the SMAD2, SMAD3, SMAD4, and increased SMAD7. Conclusion: Quercetin has anti-inflammation, antioxidant, antifibrosis activity in the CKD cells model. Thus, quercetin is a promising substance for CKD therapy and further research is needed to prove this in CKD animal model.