Moringa oleifera (M. oleifera) Lam. (family Moringaceae) possesses anti-inflammatory, anticancer, anti-diabetic, neuroprotective, and cardioprotective properties. The present review aimed to explore the protective effects of M. oleifera Lam. against metabolic disorders and to serve as a guide for future research on this medicinal plant. Research data on the anti-diabetic and anti-obesity properties of M. oleifera Lam. were collected from Science Direct, PubMed, Springer, Google Scholar, Web of Science, etc. M. oleifera has a protective effect against metabolic disorders through the modulation of various signaling pathways involved in glucose and lipid metabolism. Specifically, M. oleifera enhances insulin sensitivity by activating insulin receptor phosphorylation and the PI3K/Akt pathway, which promotes glucose uptake by facilitating GLUT-4 translocation to the cell membrane. In addition, it improves energy homeostasis and lipid metabolism by modulating the AMPK pathway. Inhibition of inflammatory biomarkers (nuclear factor kappa B, tumor necrosis factor-α, interleukin-1β, monocyte chemoattractant protein-1) and lipid peroxidation markers (malondialdehyde, F2-isoprostanes), along with enhanced activity of antioxidant enzymes (glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase), contributes to its anti-diabetic and anti-obesity effects. This review suggests that M. oleifera Lam. modulates key signaling pathways involved in glucose and lipid metabolism and holds promise as a potential therapeutic agent for managing metabolic diseases.
Objective: To investigate the protective effects of naringin on doxorubicin (DOX)-induced liver injury.
Methods: A total of 50 male rats were allocated into five groups: the control group, the DOX group, the DOX groups treated with 50 mg/kg and 100 mg/kg of naringin by gastric lavage for 10 days, as well as the group treated with 100 mg/kg of naringin alone. Liver and serum samples were collected for biochemical, histopathological, and molecular analyses, including liver enzyme activity, oxidative stress markers, inflammation, apoptosis-related proteins, and DNA damage indicators.
Results: Naringin attenuated DOX-induced elevation in liver enzyme activity and inflammation markers while enhancing antioxidant activities. Naringin also activated the Nrf2-HO-1 signaling pathway, with the most pronounced effect in the high-dose naringin group. In addition, naringin modulated apoptotic signaling by downregulating the expression of PI3K-AKT and BAX, and upregulating Bcl-2, as well as reduced the level of 8-OHdG. Histopathological evaluation showed that DOX-induced structural liver alterations, such as cellular degeneration and necrosis, were notably attenuated by naringin treatment.
Conclusions: Naringin treatment exerts protective effects against DOX-induced liver injury through its antioxidative, anti-inflammatory, and anti-apoptotic effects.
Objective: To examine the protective effect of saikosaponin D against streptozotocin (STZ)-induced gestational diabetes mellitus in female rats.
Methods: Intraperitoneal administration of STZ (40 mg/kg) was used for the induction of diabetes in pregnant rats, and rats orally received sikosaponin D (10, 20, and 40 mg/kg). The body weight, placental weight, fetal weight, fetal index, and various biochemical parameters, including antioxidant, glucose level, cytokines, and apoptosis parameters, were estimated. The expression levels of various mRNAs were also analyzed.
Results: Saikosaponin D increased body weight and fetal weight while decreasing placental weight and placental index. Saikosaponin D significantly altered various biochemical parameters such as fasting blood glucose, glycated hemoglobin (HbA1c), hemoglobin, hepatic glycogen, advanced glycation end products, lipid parameters (total cholesterol, triglyceride, low density lipoprotein, high density lipoprotein, very low density lipoprotein), antioxidant parameters (superoxide dismutase, glutathione, glutathione peroxidase, malonaldehyde, catalase), inflammatory cytokines (tumor necrosis factor-a, interleukin-6, interleukin-1β, interleukin-10), apoptosis parameters (Bcl-2, Bax, caspase-3), resistin, adiponectin, leptin, intercellular adhesion molecule 1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1. Furthermore, saikosaponin D modulated the mRNA expression of TLR4, MyD88, NF-κB, NLRP3, TNF-α, 1L-6, CRP, SIRT1, and MAPK.
Conclusions: Saikosaponin D exhibits a protective effect against STZ-induced gestational diabetes mellitus in rats via regulation of TLR4/ MyD88/NF-κB and MAPK signaling pathways.