Curcumin protects against aging-related stress and dysfunction through autophagy activation in rat brain
- PMID: 38796662
- DOI: 10.1007/s11033-024-09639-7
Curcumin protects against aging-related stress and dysfunction through autophagy activation in rat brain
Abstract
Background: Curcumin (Curcuma longa) is a well-known medicinal plant that induces autophagy in various model species, helping maintain cellular homeostasis. Its role as a caloric restriction mimetic (CRM) is being investigated. This study explores the potential of curcumin (CUR), as a CRM, to provide neuroprotection in D galactose induced accelerated senescence model of rats through modulation of autophagy. For six weeks, male rats received simultaneous supplementation of D-gal (300 mg/kg b.w., subcutaneously) and CUR (200 mg/kg b.w., oral).
Method and results: The oxidative stress indices, antioxidants, and electron transport chain complexes in brain tissues were measured using standard methods. Reverse transcriptase-polymerase chain reaction (RT-PCR) gene expression analysis was used to evaluate the expression of autophagy, neuroprotection, and aging marker genes. Our results show that curcumin significantly (p ≤ 0.05) enhanced the level of antioxidants and considerably lowered the level of oxidative stress markers. Supplementing with CUR also increased the activity of electron transport chain complexes in the mitochondria of aged brain tissue, demonstrating the antioxidant potential of CUR at the mitochondrial level. CUR was found to upregulate the expression of the aging marker gene (SIRT-1) and the genes associated with autophagy (Beclin-1 and ULK-1), as well as neuroprotection (NSE) in the brain. The expression of IL-6 and TNF-α was downregulated.
Conclusion: Our findings demonstrate that CUR suppresses oxidative damage brought on by aging by modulating autophagy. These findings imply that curcumin might be beneficial for neuroprotection in aging and age-related disorders.
Keywords: Aging; Autophagy; Caloric restriction mimetics; Curcumin; D-galactose; Neuroprotection.
© 2024. The Author(s), under exclusive licence to Springer Nature B.V.
References
-
- Guo J, Huang X, Dou L et al (2022) Aging and aging-related diseases: from molecular mechanisms to interventions and treatments. Sig Transduct Target Ther 7:391. https://doi.org/10.1038/s41392-022-01251-0 - DOI
-
- Gao H-M, Zhou H, Hong J-S (2014) Oxidative stress, Neuroinflammation, and Neurodegeneration. In: Peterson PK, Toborek M (eds) Neuroinflammation and Neurodegeneration. Springer New York, New York, NY, pp 81–104 - DOI
-
- Kamboj SS, Kumar V, Kamboj A, Sandhir R (2008) Mitochondrial oxidative stress and dysfunction in Rat Brain Induced by Carbofuran exposure. Cell Mol Neurobiol 28:961–969. https://doi.org/10.1007/s10571-008-9270-5 - DOI - PubMed
-
- Sena LA, Chandel NS (2012) Physiological roles of mitochondrial reactive oxygen species. Mol Cell 48:158–167. https://doi.org/10.1016/j.molcel.2012.09.025 - DOI - PMC - PubMed
-
- Lee C, Longo V (2016) Dietary restriction with and without caloric restriction for healthy aging. F1000Res 5:117. https://doi.org/10.12688/f1000research.7136.1 - DOI
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical