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Abstract Background Hyperlipidemia is a major cause for atherosclerosis which is a frontline cause for mortality in the world. Bisflavonoids are dimeric flavonoids abundant in few medicinal herbs with various pharmacological effects. However, in vivo anti-hyperlipidemic role of bisflavonoids (BFR) is limited. The present investigation is aimed to study BFR from the leaf extract of Araucaria bidwillii Hook. in rat model of hyperlipidemia. Results Administration of HFD was significantly (p < 0.0001) shown to increase total cholesterol (TC), low-density lipoprotein (LDL), and triglycerides (TG) associated with decrease in HDL. BFR at two doses significantly decreased TC, LDL, and TG in HFD-fed rats. In addition, BFR significantly (p < 0.0001) decreased the MDA and significantly (p < 0.0001) increased the impaired anti-oxidant enzyme SOD and CAT in heart tissue induced by HFD. Further, 28 days administration of BFR significantly (p < 0.001) decreased HFD-induced aortic wall thickness. Conclusion It can be concluded that bisflavonoids from A. bidwillii Hook. leaf extract administered to high fat-fed rats showed beneficial anti-hyperlipidemic effect by reducing lipid profiles and protecting the heart tissue from oxidative stress.

Schizophrenia is a complex psychiatric disorder associated with positive (delusion, hallucination, and disorganised speech) and negative (affective flatering, avolition and social withdrawal) symptoms. Agomelatine (AGO) has been used as an anti-depressant to improve the negative symptoms in schizophrenia patients with co-morbid major depressive disorder. Therefore, the present study aimed to investigate the anti-psychotic effect of AGO in ketamine (KET)-induced psychosis rat model. Four groups (n = 12/ group) of wistar rats were administered normal saline, KET (20 m/kg, i.p) and KET + AGO (20 and 40 mg/kg, i.p) for seven days. Behavioural tests were conducted on the seventh day after drug administration. Seven days administration of AGO at two different doses decreased the KET induced stereotypic and ataxic behaviour as compared with KET treated rats. In addition, AGO increased the social interaction time and decreased the horizontal and vertical locomotor behaviour in KET treated rats. Histologically, KET adminstration decreased hippocampal and increased basolateral amygdala (BLA) neuronal counts. AGO administration (at two different doses) significantly reversed the KET induced neuronal loss in the two brain areas. These findings suggest that AGO has a protective effect against KET-induced psychosis in this rat model. This study warrants further research to delineate the possible role of AGO in experimental model of psychosis particularly neurochemical and neuromolecular aspects.