Myocardial infarction (MI) is the most prevalent cause of cardiovascular death. A possible way of preventing MI maybe by dietary supplements. The present study was thus designed to ascertain the cardio-protective effect of a formulated curcumin and nisin based poly lactic acid nanoparticle (CurNisNp) on isoproterenol (ISO) induced MI in guinea pigs. Animals were pretreated for 7 days as follows; Groups A and B animals were given 0.5 mL/kg of normal saline, group C metoprolol (2 mg/kg), groups D and E CurNisNp 10 and 21 mg/kg respectively (n = 5). MI was induced on the 7^thday in groups B-E animals. On the 9^thday electrocardiogram (ECG) was recorded, blood samples and tissue biopsies were collected for analyses. Toxicity studies on CurNisNp were carried out. MI induction caused atrial fibrillation which was prevented by pretreatment of metoprolol or CurNisNp. MI induction was also associated with increased expressions of cardiac troponin I (CTnI) and kidney injury molecule-1 (KIM-1) which were significantly reduced in guinea pig’s pretreated with metoprolol or CurNisNp (P < 0.05). The LC₅₀of CurNisNp was 3258.2 μg/mL. This study demonstrated that the formulated curcumin-nisin based nanoparticle confers a significant level of cardio-protection in the guinea pig and is nontoxic.

Background: Mechanistic studies indicate that adenosine receptor antagonism may not account for the mechanism of caffeine's cardiovascular action in chronic caffeine users. We, thus, aimed at examining the possible role of catecholamine mechanism in caffeine's cardiovascular action during habitual use. Materials and Methods: Adult male New Zealand rabbits were divided into three groups ( n = 5). Group I rabbits were untreated and served as control whereas groups II and III rabbits were administered with 2 and 6 mg/kg caffeine, respectively, for 28 days. After anesthesia arterial pressure, electrocardiogram and heart rate were recorded. Blood and cardiac tissue samples were collected for analysis. Results: After 28 days of caffeine treatment, cardiovascular parameters were significantly altered. There were increases in catecholamine level, beta-1 receptor expression, adenylate cyclase 9 immuno-reactivity, and cardiac cyclic adenosine monophosphate concentrations. Conclusion: This study demonstrates that caffeine's cardiovascular action in rabbits involves the activation of the beta-1 adrenergic pathway.

Jatropha tanjorensis has been employed to treat various diseases. This study aimed to investigate the mode of action of J. tanjorensis against liver fibrogenesis induced by carbon tetrachloride (CCl₄). Liver fibrosis was induced in male Wistar rats by exposing them to CCl₄ for nine weeks. From weeks 7 to 9, J. tanjorensis extract was administered. The study evaluated the activities of antioxidant enzymes and lipid peroxidation (LPO) levels, expression of TGFβ1 and fibrosis-associated proteins, and liver histology. J. tanjorensis significantly increased the depleted antioxidant activities induced by CCl₄ while significantly reducing the elevated LPO levels caused by CCl₄. Furthermore, it downregulated the upregulation of TGFβ1 and fibrosis-associated proteins induced by CCl₄ and mitigated the liver lesions and collagen deposits resulting from CCl₄ exposure. Overall, J. tanjorensis alleviated liver injury and fibrogenesis by exerting its antioxidant effect and inhibition of TGFβ1.

ABSTARCTThe present study investigates the neuroprotective effects of Cannabidiol (CBD) in olanzapine/high-fat diet (HFD) treated adult male Wistar rats. Animals weighing 160-180 g were divided into five groups (n = 7). They include Untreated, HFD+Olan, Met + HFD+Olan, CBD (10 mg/kg)+HFD+Olan, and CBD (25 mg/kg)+HFD + Olan. Olanzapine and metformin were administered as 5 mg/kg and 20 mg/kg, respectively. Cognitive functions, brain biochemical markers, histology and immunohistochemistry were determined. 2 weeks cotreatment of olanzapine/HFD induced cognitive impairment evidenced by significant reduction in Object location memory (OLM) from 3.5 ± 0.75 to -39 ± 8.57% and Object recognition memory (ORM) indices from 21.47 ± 12.68 to -30.30 ± 4.29%, increased serum amyloid beta 1-42 and GFAP hypothalamic and prefrontal cortex expressions. CBD comparable to metformin ameliorated the induced cognitive impairment. CBD possesses remarkable cognitive preserving activity which is associated with decreased lipid peroxidation and down regulation of GFAP/ACHE pathway.