Methanol leaf extract of Leptadenia hastata ameliorates chronic, unpredictable, mild stress-induced depression

Dr. Ibrahim H. Sani; Dr. Muhammad A. Umar; Abdullahi Rabiu Abubakar Rabiu Abubakar; Prof. Sani Malami; Prof. Abdullahi Hamza Yaro

doi:10.54117/jcbr.v4i1.3

Authors

Dr. Ibrahim H. Sani Yusuf Maitama Sule University, Kano
Muhammad A. Umar Departments of Human Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Yusuf Maitama Sule University, Kano
Abdullahi Rabiu Abubakar Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Bayero University Kano, Nigeria
Sani Malami Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Bayero University Kano, Nigeria
Abdullahi Hamza Yaro Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Bayero University Kano, Nigeria.,

DOI:

https://doi.org/10.54117/jcbr.v4i1.3

Keywords:

Leptadenia hastata, Stress, Cortisol, Depression, Behaviour

Abstract

Leptadenia hastata (Pers) Decne is a tropical herb widely used in the phytotherapy of neuropsychiatric disorders, including depression. Despite the availability of synthetic antidepressant drugs, depression remains a major medical problem. The study aimed to evaluate the effect of methanol leaf extract of Leptadenia hastata (LHME) on chronic unpredictable mild stress-induced depression. Acute toxicity of Leptadenia hastata was determined using Organization for Economic Co-operation and Development (OECD) guidelines. The chronic unpredictable mild stress (CUMS) model-induced depression involves the evaluation of baseline behavioural changes in the sucrose preference test, open field test, and tail suspension test. The brain-derived neurotrophic factor (BDNF) concentrations and serum cortisol were assessed using an enzyme-linked immunosorbent assay (ELISA). The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were also assessed using standard procedure.

The median lethal dose (LD₅₀) value was > 5000 mg/kg. LHME at doses of 250 – 1000 mg significantly (p<0.01) decreased CUMS-induced depression in a dose-dependent manner. LHME significantly (p<0.01) reversed depression associated weight loss from 14.00±0.62 g in week two to 22.57±1.13 g in week five of the experiment. It also increased sucrose consumption in the sucrose preference test (SPT) from 4.29±0.52 ml in week two to 9.71±0.68 ml in week five. The LHME also significantly (p<0.01) decreased the duration of immobility from 190.00±4.55 sec in week two to 158.00±3.83 sec in week five in the tail suspension test (TST). Furthermore, LHME at the tested dose significantly (p<0.01) increased the locomotor activity from 36.29±1.25 sec in week two to 62.43±1.73 sec in week five in the open field test (OFT). LHME significantly (p<0.01) and dose-dependently increased the levels of BDNF (204.74±22.97 pg/ml) and decreased the levels of plasma cortisol (0.98±0.06 ng/ml). However, treatment with LHME and the standard drug imipramine did not significantly change SOD activity and the MDA level in CUMS-induced mice.

The findings demonstrated that LHME ameliorates CUMS-induced depressive-like behaviours, and its effect is possibly mediated via the neuroendocrine (cortisol) and neurotrophic (BDNF).