The effects of Moringa oleifera on blood glucose levels: A scoping review of the literature.

Diabetes is an increasingly problematic health concern in the United States. Moringa oleifera (M. oleifera) has been suggested as medication in the prevention or treatment of diabetes, but there is no convincing evidence of a causal relation between moringa and decreased blood sugar levels in humans. The purpose of this scoping review is to examine the effects of Moringa oleifera on blood glucose levels in rats and humans. A search of Scopus, Ovid Medline, Ovid Embase, IPA, and Web of Science and manual searching of bibliographies were performed for peer-reviewed English articles published between May 1, 2008 and May 1, 2018. This review included thirty studies. Out of seven human studies, five found that M. oleifera significantly reduced blood glucose levels in diabetic patients. Out of twenty-three animal studies, twenty-one found that administration of M. oleifera led to a statistically significant decrease in animal blood glucose levels. In human studies, moringa was mostly administered in a powdered leaf form, while in animal studies it was frequently administered to as an aqueous or ethanol-based extract. The review found statistical evidence that moringa decreased blood glucose; the evidence is not strong enough to recommend it as the default treatment for people with diabetes.

Heme oxygenase-1 mitigates ferroptosis in renal proximal tubule cells.

Ferroptosis is an iron-dependent form of regulated nonapoptotic cell death, which contributes to damage in models of acute kidney injury (AKI). Heme oxygenase-1 (HO-1) is a cytoprotective enzyme induced in response to cellular stress, and is protective against AKI because of its antiapoptotic and anti-inflammatory properties. However, the role of HO-1 in regulating ferroptosis is unclear. The purpose of this study was to elucidate the role of HO-1 in regulating ferroptotic cell death in renal proximal tubule cells (PTCs). Immortalized PTCs obtained from HO-1+/+ and HO-1-/- mice were treated with erastin or RSL3, ferroptosis inducers, in the presence or absence of antioxidants, an iron source, or an iron chelator. Cells were assessed for changes in morphology and metabolic activity as an indicator of cell viability. Treatment of HO-1+/+ PTCs with erastin resulted in a time- and dose-dependent increase in HO-1 gene expression and protein levels compared with vehicle-treated controls. HO-1-/- cells showed increased dose-dependent erastin- or RSL3-induced cell death in comparison to HO-1+/+ PTCs. Iron supplementation with ferric ammonium citrate in erastin-treated cells decreased cell viability further in HO-1-/- PTCs compared with HO-1+/+ cells. Cotreatment with ferrostatin-1 (ferroptosis inhibitor), deferoxamine (iron chelator), or N-acetyl-l-cysteine (glutathione replenisher) significantly increased cell viability and attenuated erastin-induced ferroptosis in both HO-1+/+ and HO-1-/- PTCs. These results demonstrate an important antiferroptotic role of HO-1 in renal epithelial cells.