THE AIM OF THE STUDY: To investigate the effects of the chronic (28 days) oral administration of CT root extract on CCH-induced cognitive impairment, neuronal damage and cholinergic deficit, and its toxicity profile in the CCH rat model.
MATERIALS AND METHODS: The permanent bilateral occlusion of common carotid arteries (PBOCCA) surgery method was employed to develop a CCH model in male Sprague Dawley (SD) rats. Then, these rats were given oral administration of CT root extract at doses of 100, 200, and 300 mg/kg, respectively for 28 days and subjected to behavioural tests. At the end of the experiment, the brain was harvested for histological analysis and cholinesterase activities. Then, blood samples were collected and organs such as liver, kidney, lung, heart, and spleen were procured for toxicity assessment.
RESULTS: Chronic treatment of CT root extract at doses of 200 and 300 mg/kg, restored memory impairments induced by CCH. CT root extract was also found to diminish CCH-induced neuronal damage in the CA1 region of the hippocampus. High dose (300 mg/kg) of the CT root extract was significantly inhibited the increased acetylcholinesterase (AChE) activity in the frontal cortex and hippocampus of the PBOCCA rats. In toxicity study, repeated doses of CT root extract were found to be safe in PBOCCA rats after 28 days of treatment.
CONCLUSIONS: Our findings provided scientific evidence supporting the therapeutic potential of CT root extract in the treatment of vascular dementia (VaD)-related cholinergic abnormalities and subsequent cognitive decline.
METHODS: Thirty healthy adult male Wistar rats (150-180 g) were randomly divided into three groups which included control (C; n = 6), PA extract (PAE; n = 6) and Metabolic Syndrome (MetS; n = 18). Food and fluid were given ad libitum for 8 weeks. These groups differed in fluid intake whereby rats received tap water, 10% of PA leaf water extracts and 20% of fructose in drinking water in group C, PAE and MetS, respectively. After 8 weeks, the MetS group was further subdivided into three subgroups namely MetS1 (n = 6), MetS2 (n = 6) and MetS3 (n = 6). The C, PAE and MetS1 were sacrificed. MetS1 group was sacrificed as the control for metabolic syndrome. MetS2 and MetS3 groups were treated with only tap water and 10% of PA leaf water extract respectively for another 8 weeks. The parameters for physiological and metabolic changes such as obesity, hypertension, hyperglycaemia, dyslipidaemia, and inflammatory biomarkers (NFκβ p65, TNFα, leptin and adiponectin) were measured.
RESULTS: The intake of 20% of fructose in drinking water induced full blown of metabolic syndrome symptoms, including obesity, hypertension, dyslipidaemia and hyperglycaemia in male Wistar rats. Subsequently, treatment with PA leaf water extract improved obesity parameters including BMI, abdominal adipose tissue deposition and adipocytes size, systolic and diastolic blood pressures, fasting plasma glucose, triglycerides, high density lipoprotein with neutral effects on inflammatory biomarkers.
CONCLUSIONS: Administration of PA in metabolic syndrome rat model attenuates most of the metabolic syndrome symptoms as well as improves obesity. Therefore, PA which is rich in total flavonoids and total phenolic acids can be suggested as a useful dietary supplement to improve metabolic syndrome components induces by fructose.