Volume : 13, Issue : 01, January – 2026
Title:
ANTIDEPRESSANT ACTIVITY OF MESUA FERREA AGAINST RESERPINE-INDUCED DEPRESSION IN MICE
Authors :
Papagatla Poli Reddy*, Chepuri Neha
Abstract :
The present study was designed to evaluate the antidepressant and antioxidant potential of Mesua ferrea extract in Reserpine-induced depressive rodent models. Behavioral assessments, including the Forced Swim Test (FST), Tail Suspension Test (TST), and Open Field Test (OFT), were conducted to assess depressive-like behavior, locomotor activity, and exploratory behavior. Biochemical parameters, including liver enzymes (ALT, AST, ALP), lipid profile (cholesterol, triglycerides, HDL, LDL), glucose levels, and oxidative stress markers (MDA, SOD, catalase, GSH), were analyzed to evaluate metabolic, hepatic, and antioxidant effects. Reserpine administration induced significant depressive-like behavior, hepatic stress, dyslipidemia, hyperglycemia, and oxidative stress. Treatment with Mesua ferrea extract significantly reduced immobility time in FST and TST, improved locomotor and exploratory activity in OFT, normalized liver enzymes and lipid/glucose levels, and restored antioxidant status in a dose-dependent manner, with the 500 mg/kg dose showing the most pronounced effects. These findings suggest that Mesua ferrea extract possesses antidepressant, hepatoprotective, and antioxidant properties, highlighting its potential as a natural therapeutic agent for managing depression.
Keywords: Mesua ferrea, Antidepressant activity, Liver enzymes, Lipid profile, Reserpine-induced depression.
Cite This Article:
Please cite this article in press Papagatla Poli Reddy et al., Antidepressant Activity Of Mesua Ferrea Against Reserpine-Induced Depression In Mice, Indo Am. J. P. Sci, 2026; 13(01).
REFERENCES:
1. Disease, G. B. D., Injury, I. & Prevalence, C. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 392, 1789–1858 (2018).
2. Nagy, C. et al. Single-nucleus transcriptomics of the prefrontal cortex in major depressive disorder implicates oligodendrocyte precursor cells and excitatory neurons. Nat. Neurosci. 23, 771–781 (2020).
3. Malhi, G. S. & Mann, J. J. Depression Lancet 392, 2299–2312 (2018).
4. Fellinger, M. et al. Seasonality in major depressive disorder: effect of sex and age. J. Affect Disord. 296, 111–116 (2022).
5. Liu, C. H. et al. Role of inflammation in depression relapse. J. Neuroinflammation 16, 90 (2019).
6. Burcusa, S. L. & Iacono, W. G. Risk for recurrence in depression. Clin. Psychol. Rev. 27, 959–985 (2007).
7. Monroe, S. M. & Harkness, K. L. Life stress, the “kindling” hypothesis, and the recurrence of depression: considerations from a life stress perspective. Psychol. Rev. 112, 417–445 (2005).
8. Albert, K. M. & Newhouse, P. A. Estrogen, stress, and depression: cognitive and biological interactions. Annu. Rev. Clin. Psychol. 15, 399–423 (2019).
9. Kessler, R. C., Chiu, W. T., Demler, O., Merikangas, K. R. & Walters, E. E. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch. Gen. Psychiatry 62, 617–627 (2005).
10. Monteleone, P. & Maj, M. The circadian basis of mood disorders: recent devel opments and treatment implications. Eur. Neuropsychopharmacol. 18, 701–711 (2008).
11. Rice, F. et al. Adolescent and adult differences in major depression symptom profiles. J. Affect Disord. 243, 175–181 (2019).
12. Hasin, D. S. et al. Epidemiology of adult DSM-5 major depressive disorder and its specifiers in the United States. JAMA Psychiatry 75, 336–346 (2018).
13. Howard, D. M. et al. Genome-wide association study of depression phenotypes in UK Biobank identifies variants in excitatory synaptic pathways. Nat. Commun. 9, 1470 (2018).
14. Kovacs, M. & Lopez-Duran, N. Prodromal symptoms and atypical affectivity as predictors of major depression in juveniles: implications for prevention. J. Child Psychol. Psychiatry 51, 472–496 (2010).
15. Stetler, C. & Miller, G. E. Depression and hypothalamic-pituitary-adrenal activa tion: a quantitative summary of four decades of research. Psychosom. Med. 73, 114–126 (2011).
16. Milaneschi, Y., Lamers, F., Berk, M. & Penninx, B. Depression heterogeneity and its biological underpinnings: toward immunometabolic depression. Biol. Psy chiatry 88, 369-380 (2020)
17. Zhou, X. et al. Astrocyte, a promising target for mood disorder interventions. Front. Mol. Neurosci. 12, 136 (2019).
18. Monroe, S. M. & Harkness, K. L. Major depression and its recurrences: life course matters. Annu. Rev. Clin. Psychol. 18, 329–357 (2022).
19. Wray, N. R. et al. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression. Nat. Genet. 50, 668–681 (2018).
20. Gittins, R. A. & Harrison, P. J. A morphometric study of glia and neurons in the anterior cingulate cortex in mood disorder. J. Affect. Disord. 133, 328–332 (2011). \
21. Miguel-Hidalgo, J. J. et al. Glial and glutamatergic markers in depression, alco holism, and their comorbidity. J. Affect. Disord. 127, 230–240 (2010).
22. Sequeira, A. et al. Global brain gene expression analysis links glutamatergic and GABAergic alterations to suicide and major depression. PLoS ONE 4, e6585 (2009).
23. Rajkowska, G. & Stockmeier, C. A. Astrocyte pathology in major depressive disorder: insights from human postmortem brain tissue. Curr. Drug Targets 14, 1225–1236 (2013).
24. Rajalakshmi B, Rajani V, Raju CN, Bhongiri B. The phytochemical investigation and pharmacological evaluation of hepatoprotective activity of Bougainvillea glabra in rats. Current Trends in Biotechnology and Pharmacy. 2024;18(1):1574-80.