Evidence is provided that dietary quinoa beneficially modulates renal molecular pathways involved in oxidative stress and inflammatory responses under physiological conditions.
Abstract
Oxidative stress and inflammation contribute to renal dysfunction, and antioxidant-rich functional foods may modulate these processes. This study evaluated the effects of dietary quinoa on oxidative stress and the expression of pyroptosis, inflammation and apoptosis-related genes in healthy rat kidneys. Forty male Wistar albino rats were randomly assigned to control and diet groups containing 5%, 10% or 20% quinoa for six weeks (n=10). Rat body weight, superoxide dismutase activity, glutathione, and malondialdehyde levels in kidney tissue were measured; expression of nine genes was assessed in a representative subgroup using quantitative real-time polymerase chain reaction. Quinoa dose-dependently increased antioxidant markers, reduced lipid peroxidation, and downregulated inflammasome (Nlrp3, Casp-1,Gsdmd), inflammatory (Nf-κB, IL-1β, Tnf-α), and apoptotic (Bax,Casp-3) genes, while increasing Bcl2 expression, with the greatest effects at 10% and 20% quinoa. These findings provide evidence that dietary quinoa beneficially modulates renal molecular pathways involved in oxidative stress and inflammatory responses under physiological conditions.
ABSTRACT Introduction Type 2 diabetes mellitus (T2DM) is strongly associated with oxidative stress and inflammation. Harmaline (HAR), an alkaloid with antioxidant and anti‐inflammatory properties, has been suggested to possess antidiabetic potential. This study investigated the effects of HAR in experimental T2DM and its association with changes in the nuclear factor erythroid 2‐related factor 2 (Nrf2) and nuclear factor kappa‐B (NF‐κB) pathways. Methods In vitro experiments were performed using mouse pancreatic cells cultured under different glucose concentrations to evaluate insulin secretion and antioxidant status. For the in vivo study, T2DM was induced in mice by nicotinamide (120 mg/kg) and streptozotocin (65 mg/kg). Fasting blood glucose (FBG) was measured 1 week after induction. Forty‐eight adult male NMRI mice were randomly assigned to four groups: normal control (NC), diabetic control (DC), HAR‐treated (30 mg/kg), and metformin‐treated (150 mg/kg). Treatments were administered once daily for 10 days. Results HAR enhanced insulin secretion and antioxidant capacity while reducing lipid peroxidation in vitro. In diabetic mice, HAR significantly reduced FBG, improved the lipid profile, and restored pancreatic antioxidant status. These effects were accompanied by increased expression of miR‐200a, Nrf2, and NAD(P)H: quinone oxidoreductase 1 and reduced Keap1 expression. In addition, HAR increased miR‐125b expression and reduced the expression of NF‐κB, TNF‐α, IL‐1β, and IL‐6. Decreased changes in RAS‐related markers were also observed after HAR treatment. Conclusion HAR improved glycemic control and pancreatic antioxidant status and reduced inflammatory responses in experimental T2DM. These beneficial effects were associated with modulation of Nrf2, NF‐κB, and RAS‐related signalling pathways, suggesting their potential involvement in the observed protective effects. Further studies are needed to establish the underlying mechanisms and evaluate the long‐term efficacy and safety of HAR.
Objective(s): Atherosclerosis (AS) is caused by dyslipidemia, chronic inflammation, and oxidative stress. Ponicidin, a diterpenoid from Isodon species, has reported anti-inflammatory and antioxidant effects, but its role in AS remains unclear. In this study, we evaluated the therapeutic potential and safety of ponicidin in an experimental AS model. Materials and Methods: ApoE-/- mice were fed a Western diet and treated with ponicidin (10 mg/kg/day, intraperitoneally) for 12 weeks. Hepatic and renal safety were assessed using histological and serum biochemical markers. Aortic plaque burden was quantified using hematoxylin and eosin and Oil Red O staining. Plasma lipids, cytokines, oxidative stress markers, and antioxidant enzymes were measured using biochemical assays and ELISA. The effects on SIRT1 and PI3K/Akt/eNOS signaling were analyzed using immunohistochemistry, RT-qPCR, ELISA, and Western blotting. Results: Ponicidin showed no liver or kidney toxicity and moderately altered the body weight. Treatment significantly reduced aortic root plaque coverage and lesion area while improving plasma lipid profiles (↓TG, ↓TC, ↓LDL-C, and ↑HDL-C). Serum cytokine analysis revealed decreased TNF-α, IL-1β, IL-6, MCP-1, and TGF-β1 levels, with elevated IL-10. Oxidative stress was attenuated, as evidenced by reduced malondialdehyde and myeloperoxidase levels, increased superoxide dismutase, catalase, and glutathione levels, and restored nitric oxide levels. Mechanistically, ponicidin up-regulated SIRT1 expression and enhanced the phosphorylation of PI3K, Akt, and eNOS, suggesting improved endothelial function. Conclusion: Ponicidin protects against AS by improving lipid metabolism, reducing vascular inflammation and oxidative stress, and enhancing endothelial signaling.
Kang Ye, Jing Shi, Ping Gong et al.· Iranian Journal of Basic Med...· 0 citations
Background:Persistent oxidative stress and chronic low-grade inflammation are hallmarks of diabetes mellitus, and both are important factors in the onset and course of diabetic complications. Although frankincense (Boswellia sacra) is widely known for its anti-inflammatory and antioxidant properties, its coordinated effects on pro- and anti-inflammatory mediators in the context of diabetes remain poorly understood.Methods:Three groups of adult male Sprague-Dawley rats were randomly assigned: 10 healthy control rats, 15 diabetic control rats, and 15 diabetic rats administered oral frankincense extract (500 mg/kg/day) for 28 days. Type 2 diabetes mellitus was induced in the designated groups by a single intraperitoneal injection of streptozotocin (STZ; 55 mg/kg). On days 14 and 28, serum samples were collected to measure antioxidant indicators, including glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF), serum amyloid A (SAA), C-reactive protein (CRP), and interleukin-10 (IL-10) were among the inflammatory and regulatory biomarkers evaluated. Histopathological samples were collected from the liver, kidneys, and pancreas on day 28 of the experiment.Results:Diabetic controls exhibited significant reductions in CAT, SOD, and GPx activities compared with healthy controls (p < 0.05), alongside elevated MDA, CRP, SAA, TNF-α, and IL-1β (p < 0.05). Frankincense supplementation for 28 days significantly increased CAT (101.3 ± 19.11 U/L) and GPx (39.39 ± 0.93 mU/mL) compared with diabetic controls (64.14 ± 1.25 U/L and 20.43 ± 0.97 mU/mL; p < 0.05 and 0.001, respectively). MDA levels were reduced from 17.4 ± 0.82 to 9.44 ± 0.29 nmol/mL (p < 0.001). CRP and SAA decreased markedly to 50.4 ± 2.08 U/L and 9.65 ± 0.40 ng/mL, respectively (p < 0.01 vs. diabetic controls). TNF-α was significantly reduced to 14.11 ± 0.98 pg/mL on day 14 (p < 0.001), but returned to levels comparable to untreated diabetic rats by day 28. At the end of the experiment, Frankincense supplementation significantly elevated TGF-β levels (p < 0.01) but did not significantly alter CTGF levels, while IL-10 levels decreased significantly (p < 0.001). Frankincense ameliorated and partially restored the adverse histopathological findings of diabetes in rats, including hepatocyte swelling and fatty degeneration, glomerular hemorrhage and inflammation, and pancreatic injury.Conclusions:Frankincense supplementation at 500 mg/kg for 28 days effectively attenuates diabetes-induced oxidative stress by restoring antioxidant activities and reducing lipid peroxidation, while suppressing key proinflammatory mediators. These findings support the further investigation of frankincense as an adjunctive strategy for managing the oxidative and inflammatory burden associated with diabetes.
F. Alshanbari, Aka Zaki, Y. Alharbi et al.· International Journal of Pha...· 0 citations
The liver is highly susceptible to oxidative stress and systemic inflammation that may be triggered by L-ornithine-induced acute pancreatitis. The accumulation of reactive oxygen species (ROS) causes redox imbalance, increases lipid peroxidation, and depletes endogenous antioxidants such as glutathione (GSH), while reducing the activity of antioxidant enzymes such as superoxide dismutase (SOD). This study investigated whether vitamins C and K2 could protect against L-ornithine-induced hepatic injury, either separately or in combination, by enhancing antioxidant defense, reducing lipid peroxidation, maintaining hepatocyte integrity, and attenuating histopathological liver injury. Twenty-five adult female white albino rats weighing 200–250 grams were randomly divided into five experimental groups: healthy control, L-ornithine-treated control, vitamin C-treated, vitamin K2-treated, and combined vitamin C + K2-treated groups. Liver injury was induced by a single intraperitoneal injection of L-ornithine (3 g/kg). Vitamin C (100 mg/kg) and K2 (200 mg/kg) were administered separately or in combination for one month. Blood serum and liver tissue samples were collected for biochemical and histopathological examination, respectively. L-ornithine caused a notable decrease in SOD activity and GSH levels, accompanied by an increase in malondialdehyde (MDA) levels. All three treatment groups improved these indicators of oxidative stress. Histopathological evaluation demonstrated marked inflammatory changes and disruption of the overall hepatic architecture in the L-ornithine-treated group. Vitamin C and K2 attenuated these pathological changes, while the combined treatment showed the greatest histopathological improvement. These findings suggest that vitamins C and K2 may have protective effects against L-ornithine-associated hepatic injury, with combined administration showing the greatest histopathological improvement.
Halah Hashim Dahham, Jinan Tami Shihan· Journal of Medical Science,...· 0 citations
Aims: This study aimed to examine the molecular, immunohistochemical, and histopathological impacts of zinc (ZnSO₄) supplementation on apoptosis, ferroptosis, and fibrosis pathways in the kidney tissue of aged female rats with type 2 diabetes, induced by a high-fat diet and streptozotocin (STZ). Methods: Female rats aged 18 months were allocated into four groups: Normoglycemic (NRM), normoglycemic supplemented with zinc (NRM-ZnSO₄), type 2 diabetes mellitus (T2DM), and T2DM supplemented with zinc (T2DM-ZnSO₄). Groups of diabetic subjects received 5 mg/kg/day ZnSO₄ intraperitoneally for a period of 4 weeks. The metallothionein-1a (MT-1a), transforming growth factor-beta 1 (TGF-β1), and vascular endothelial growth factor-A (VEGF-A) gene expressions were assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Protein levels of cysteine-aspartic acid protease 3 (Caspase-3), glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), and VEGF were evaluated by immunohistochemistry; cellular damage and collagen deposition were determined by periodic acid-Schiff (PAS) and Masson trichrome staining. Results: Zinc supplementation in the T2DM-ZnSO₄ group maximized MT-1a gene expression, indicating enhanced cellular antioxidant defense, and significantly reduced TGF-β1 and VEGF-A mRNA levels associated with tissue fibrosis and pathological angiogenesis (p
Nilüfer Akgün Ünal, G. Altun, Serpil Çilingiroğlu Anlı· Journal of Medicine and Pall...· 0 citations
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