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The present study describes the green biofunctional synthesis of magnesium oxide (MgO) nanoparticles using the aqueous Tarenna asiatica fruit extract. The characterization of Tarenna asiatica fruit extract MgO nanoparticles (TAFEMgO NPs) was achieved by X-ray powder diffraction, UV-Vis spectroscopy, FTIR, TEM, SEM, and energy-dispersive X-ray diffraction. TAFEMgO NPs scavenged the DPPH free radicals with an IC50 value of 55.95 μg/μL, and it was highly significant compared to the standard. To authenticate the observed antioxidant potential of TAFEMgO NPs, oxidative stress was induced in red blood cells (RBC) using sodium nitrite (NaNO2). Interestingly, TAFEMgO NPs ameliorated the RBC damage from oxidative stress by significantly restoring the stress parameters, such as the protein carbonyl content (PCC), lipid peroxidation (LPO), total thiol (TT), super-oxide dismutase (SOD), and catalase (CAT). Furthermore, oxidative stress was induced in-vivo in Sprague Dawley female rats using diclofenac (DFC). TAFEMgO NPs normalized the stress parameters in-vivo and minimized the oxidative damage in tissues. Most importantly, TAFEMgO NPs restored the function and architecture of the damaged livers, kidneys, and small intestines by regulating biochemical parameters. TAFEMgO NPs exhibited an anticoagulant effect by increasing the clotting time from 193 s in the control to 885 s in the platelet rich plasma. TAFEMgO NPs prolonged the formation of the clot process in the activated partial thromboplastin time and the prothrombin time, suggest the effective involvement in both intrinsic and extrinsic clotting pathways of the blood coagulation cascade. TAFEMgO NPs inhibited adenosine di-phosphate (ADP)-induced platelet aggregation. TAFEMgO NPs did not show hemolytic, hemorrhagic, and edema-inducing properties at the tested concentration of 100 mg/kgbody weight, suggesting its non-toxic property. In conclusion, TAFEMgO NPs mitigates the sodium nitrite (NaNO2)- and diclofenac (DFC)-induced stress due to oxidative damage in both in vitro and in vivo experimental models.

Objective: To explore the anticoagulant, antiplatelet and antioxidant activities of protein extract of kenaf seed (PEKS). Methods: Sodium dodecyl sulphate polyacrylamide gel electrophoresis and reverse-phase high-performance liquid chromatography techniques were employed for protein characterization. Antioxidant activity of PEKS was assessed using 1,1-diphenyl-2-picrylhydrazyl (DPPH) assay. The protective effect of PEKS on sodium nitrite (NaNO2) induced oxidative stress was evaluated using the in vitro red blood cell model, while the effect of PEKS on diclofenac-induced oxidative stress was examined in vivo in rats. Platelet-rich plasma and platelet-poor plasma were used for anticoagulant and antiplatelet activities of PEKS. Results: PEKS revealed similar protein bands on SDS-PAGE under reduced and non-reduced conditions. Several acidic proteins were present in native PAGE. PEKS showed antioxidant properties by scavenging DPPH with an IC50 of 24.58 μg. PEKS exhibited a protective effect on NaNO2 induced oxidative stress in red blood cells by restoring the activity of stress markers. In addition, PEKS alleviated diclofenac-induced tissue damage of the liver, kidney, and small intestine. PEKS showed an anticoagulant effect in both in vivo and in vitro experiments by enhancing normal clotting time. PEKS did not affect prothrombin time but increase activated partial thromboplastin time. Furthermore, PEKS inhibited adenosine diphosphate and epinephrine-induced platelet aggregation. Conclusions: PEKS protects tissues from oxidative stress and exhibits antithrombotic activity.