Antidepressant Effect of Cinnamon (Cinnamomum burmannii) Bark Extract in Chronic Stress-Induced Rats

Abstract

BACKGROUND: Depression is a psychiatric disorder that has become a serious health problem in the past decade. This disorder is characterized by prolonged dysphoric mood, and in more severe condition would result in decreased self-care and even life-threatening action. Serotonin is believed to play a role in the regulation of mood elation in depressive disorders. Decreased levels of serotonin in the hippocampus will cause an increased dopamine in mesolimbic dopamine neuronal cells. An effective and commonly used drug is the selective serotonin reuptake inhibitor, namely, fluoxetine. However, this agent has so many side effects, one of them is erectile dysfunction. In order to find the better treatment, exploration and discovery of therapeutic modalities need to pursued using natural materials.
 AIM: This study aimed to explore and evaluate antidepressant effects of cinnamon (Cinnamomum burmannii) extract (CE).
 METHODS: A total of 30 male Wistar rats were obtained from Eureka Research Laboratory (Palembang, Indonesia). Cinnamon simplisia was obtained from the Institute for Research and Testing of Traditional Medicine, Tawangmangu, Central Java, Indonesia. Rats were induced using chronic mild stress (CMS). CMS was a form of stress induction performed on experimental animals continuously, for 4 weeks. Forced swimming test (FST) was a test conducted to assess mobility in animal model. After induction for 4 weeks, rats were randomly divided into six groups which each contained five rats: Normal control group, CMS group (negative control), CMS + fluoxetin (Fluox 1: mg/kg), CMS + CE 25 mg/kg, the CMS + CE 50 mg/kg, and the CMS + CE 100 mg/kg. Treatment with fluoxetine or CE was given for 14 days intragastrically using gastric sonde. After treatment and FST, organ evacuation was performed and followed by immunohistochemistry and enzyme-linked immunosorbent examination.
 RESULTS: This study showed that CE with dose of 25 mg/kg BW to dose 100 mg/k BW could reduce the duration of immobility when compared to the CMS group. Clinically, CE possessed the potential to reduce the duration of immobility and potentially reduce symptoms of depression. Histologically, CE showed the potential to improve serotonin levels in the hippocampus with increasing doses. Tumor necrosis factor (TNF)-alpha expression in the hippocampus as a marker of inflammation had increased in the CMS group. CE was able to reduce the expression of TNF-alpha compared to the CMS group.
 CONCLUSION: CE possessed antidepressant efficacy by inhibiting the inflammatory process in the hippocampus so it was able to optimally increase serotonin levels in the hippocampus.