4.7 Article

Bioactive Ingredients in K. pinnata Extract and Synergistic Effects of Combined K. pinnata and Metformin Preparations on Antioxidant Activities in Diabetic and Non-Diabetic Skeletal Muscle Cells

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Publisher

MDPI
DOI: 10.3390/ijms24076211

Keywords

K. pinnata; diabetic skeletal muscle cells; oxidative stress; type II diabetes mellitus

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With rising healthcare costs, alternative medicine is becoming a popular choice for patients looking for treatment. This study investigated the effects of combining natural product Kalanchoe Pinnata (K. pinnata) with metformin on antioxidant activity in human skeletal muscle myoblasts. The results showed that the combination increased enzymatic activity and levels of antioxidants in both non-diabetic and diabetic cells, suggesting potential for treating oxidative-stress-mediated complications in type II diabetes.
With healthcare costs rising, many affected by ailments are turning to alternative medicine for treatment. More people are choosing to complement their pharmacological regimen with dietary supplements from natural products. In this study, the compound composition of Kalanchoe Pinnata (K. pinnata) and the effects of combined preparations of K. pinnata and metformin on antioxidant activity in human skeletal muscle myoblasts (HSMMs) and human diabetic skeletal muscle myoblasts (DHSMMs) were investigated. Ultraperformance liquid chromatography fusion orbitrap mass spectrometry (UPLC-OT-FTMS) identified biologically active flavanols in K. pinnata. The main compounds identified in locally grown K. pinnata were quercetin, kaempferol, apigenin, epigallocatechin gallate (EGCG), and avicularin. Antioxidant results indicated that a combinatorial preparation of K. pinnata with metformin may modulate antioxidant responses by increasing the enzymatic activity of superoxide dismutase and increasing levels of reduced glutathione. A combination of 50 mu M and 150 mu g/mL of metformin and K. pinnata, respectively, resulted in a significant increase in reduced glutathione levels in non-diabetic and diabetic human skeletal muscle myoblasts and H(2)O(2-)stress-induced human skeletal muscle myoblasts. Additionally, a K. pinnata treatment (400 mu g/mL) alone significantly increased catalase (CAT) activity for non-diabetic and diabetic human skeletal muscle myoblasts and a H(2)O(2-)stress-induced human skeletal muscle myoblast cell line, while significantly lowering malondialdehyde (MDA) levels. However, the treatment options were more effective at promoting cell viability after 24 h versus 72 h and did not promote cell viability after 72 h in H2O2-stress-induced HSMM cells. These treatment options show promise for treating oxidative-stress-mediated pathophysiological complications associated with type II diabetes.

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