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Background: The cardiovascular crisis is advancing rapidly throughout the world. A large number of studies have shown that plant polyphenols affect major mechanisms involved in cardiovascular events through their action on the antioxidant system, signaling, and transcription pathways. D-limonene, a monocyclic monoterpene obtained from citrus fruits, is reported to possess many pharmacological activities. Methods: The experiment was designed to determine the protective effect of D-limonene against cardiac injury induced by CCl4 in Wistar rats. Rats were treated with two doses of D-limonene against cardiac injury induced by CCl4. Serum toxicity markers, cardiac toxicity biomarker enzymes, inflammatory mediators, anti-oxidant armory, lipid peroxidation, lipid profile, and histology were done. Results: CCl4 intoxication resulted in a substantial rise in FFA, TC, TG, PL, LDL, VLDL, and a reduction in HDL, restoring these changes with the administration of D-limonene at a dosage of 200 mg/kg. CCl4 administration also resulted in lipid oxidation and decreased antioxidant activity. At the same time, D-limonene at a dosage of 200 mg/kg body weight inhibited LPO and restored in vivo antioxidant components to normal. CCl4 intoxication also resulted in a significant increase in inflammatory markers like IL-6, TNF-α, high sensitivity Corticotropin Releasing Factor (Hs-CRF), and biomarkers of cardiac toxicity like alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase MB (CKMB), and Troponin I & troponin-t activities. D-limonene reversed all these changes to normal. Histology further confirmed our obtained results. Conclusion: These findings indicate that D-limonene can ameliorate cardiac injury at a 200 mg/kg body weight dosage. Henceforth, D-Limonene intervenes in mediating CCl4 induced toxicity by various signaling pathways. [ABSTRACT FROM AUTHOR]

Dietary phytochemicals are important contributors to various diseases prevention, due to their interactions with CYP family enzymes. Safranal and crocin are bioactive compounds present in Crocus sativus L., commonly known as saffron. In present study, we prepared saffron extract and performed its HPLC phytochemical analysis for safranal and crocin content. We have also determined the effect of crocin and safranal on the metabolic activity of CYP2C9 by using in-silico approaches such as 3D-QSAR molecular docking and pharmacophore mapping studies. The extraction method was simple and the content of crocin and safranal was obtained to be 26.45 ± 0.03 and 11.0 ± 0.02 mg/g of saffron respectively. The predictivity of the best 3D-QSAR model developed for flavonoid derivatives was found to be 91.3%. The predicted activities of crocin and safranal for CYP2C9 were found to be 7.805 and 7.120 respectively. Further, docking studies revealed that crocin bonded CYP2C9 protein with binding affinity -9 kcal/mol, whereas, co-crystallized standard flurbiprofen bonded with 8.2 kcal/mol only. The results obtained in the present study furnish primary data for future in vitro and in vivo herb-drug interaction studies involving CYP2C9 enzyme. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the protective effect of methanol extract of Moringa oleifera leaves (MEMO) in high-fat diet (HFD)-induced dyslipidemia and vascular endothelium dysfunction. Methods: Dose-dependent attenuating effect of MEMO was tested at doses of 200 and 400 mg/kg/day in an in vivo model of HFD-induced dyslipidemia using rats whereas vascular endothelial reactivity was assessed in isolated rat aorta using ex vivo organ bath setup. Results: MEMO administration in HFD-induced dyslipidemic rats for 3 consecutive weeks, resulted in significant decrease in rat body weight, LW/BW and RFPW/BW ratio when compared to rats treated with HFD only where an increase in body weight was observed. Decrease in the average daily feed intake and significant reductions in waist, Lee index and BMI was also observed after MEMO treatment in HFD-induced dyslipidemic rats. Lipid profile data indicate that HFD group showed significant increase in total cholesterol, triglyceride, LDL and VLDL levels while HDL levels decreased significantly. On the other hand, MEMO treatment improved lipid profile compared to HFD group. Ex-vivo isolated aorta results revealed that MEMO treatment reversed HFD-induced endothelium dysfunction when compared to SD group. Conclusion: MEMO treatment produces dose-dependent improvement in lipid profile and vascular endothelium protection, thereby rationalizing its traditional medicine use in the treatment of dyslipidemia and cardiovascular related endothelial disorders. [ABSTRACT FROM AUTHOR]