Volume 29, Issue 2 (Iran South Med J 2026)
Iran South Med J 2026, 29(2): 66-78 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Haghdoost Yazdi H, Sofiabadi M, Khadem Haghighian H, Yaghoubi M. Relationship of Serum Levels of High Density Lipoprotein (HDL) and Low Density Lipoprotein (LDL) with the Severity of Parkinson's Disease in an Animal Model. Iran South Med J 2026; 29 (2) :66-78
URL: http://ismj.bpums.ac.ir/article-1-2544-en.html
URL: http://ismj.bpums.ac.ir/article-1-2544-en.html
1- Department of Physiology, School of MedIcne, Qazvin University of Medical Sciences, Qazvin, Iran
2- Department of Physiology, School of MedIcne, Qazvin University of Medical Sciences, Qazvin, Iran ,msofiabadi@qums.ac.ir
3- Department of Nutrition, School of Health, Qazvin University of Medical Sciences, Qazvin, Iran
2- Department of Physiology, School of MedIcne, Qazvin University of Medical Sciences, Qazvin, Iran ,
3- Department of Nutrition, School of Health, Qazvin University of Medical Sciences, Qazvin, Iran
Abstract: (256 Views)
Background: Parkinson's disease (PD) is the second most common neurodegenerative disease. Oxidative stress and dyslipidemia may play a key role in the pathogenesis and progression of PD. In this experimental study, the relationship of serum levels of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) with the severity of Parkinson's disease was investigated in an animal model.
Materials and Methods: Rats were divided into three groups: control, sham (vehicle injection) and parkinsonian (injection of 6-hydroxydopamine, 4 μg/μl, and volume 10 μl into the striatum). The incidence and severity of Parkinson's symptoms were assessed before and after surgery by apomorphine-induced rotation behavioral test. Blood sampling was performed once before surgery and twice after surgery (weeks 3 and 10), and serum HDL and LDL levels were measured by colorimetric methods.
Results: Pre-surgery serum LDL and HDL levels were 22.5±1.3 and 31.6±1.1 mg/dl, respectively. In the toxin-receiving group, HDL levels decreased significantly on weeks 3 and 10, while LDL levels increased significantly (P<0.01). The decrease in HDL was greater in rats with severe symptoms than in those with mild symptoms, whereas the increase in LDL was observed only in the severe symptom group.
Conclusion: Induction of Parkinson's disease by 6-hydroxydopamine toxin in rats is accompanied by changes in serum LDL and HDL levels, and these changes depend on the severity of behavioral symptoms.
Materials and Methods: Rats were divided into three groups: control, sham (vehicle injection) and parkinsonian (injection of 6-hydroxydopamine, 4 μg/μl, and volume 10 μl into the striatum). The incidence and severity of Parkinson's symptoms were assessed before and after surgery by apomorphine-induced rotation behavioral test. Blood sampling was performed once before surgery and twice after surgery (weeks 3 and 10), and serum HDL and LDL levels were measured by colorimetric methods.
Results: Pre-surgery serum LDL and HDL levels were 22.5±1.3 and 31.6±1.1 mg/dl, respectively. In the toxin-receiving group, HDL levels decreased significantly on weeks 3 and 10, while LDL levels increased significantly (P<0.01). The decrease in HDL was greater in rats with severe symptoms than in those with mild symptoms, whereas the increase in LDL was observed only in the severe symptom group.
Conclusion: Induction of Parkinson's disease by 6-hydroxydopamine toxin in rats is accompanied by changes in serum LDL and HDL levels, and these changes depend on the severity of behavioral symptoms.
Original: Original |
Subject:
Physiology
Received: 2026/04/12 | Accepted: 2026/07/18 | Published: 2026/07/29
Received: 2026/04/12 | Accepted: 2026/07/18 | Published: 2026/07/29
References
1. Kalia LV, Lang AE. Parkinson's disease. Lancet 2015; 386(9996): 896-912. [DOI]
2. Poewe W, Seppi K, Tanner CM, et al. Parkinson dis-ease. Nat Rev Dis Primers 2017; 3: 17013. [DOI]
3. Surmeier DJ, Obeso JA, Halliday GM. Selective neuronal vulnerability in Parkinson disease. Nat Rev Neurosci 2017; 18(2): 101-113. [DOI]
4. Ascherio A, Schwarzschild MA. The epidemiology of Parkinson's disease: risk factors and prevention. Lancet Neurol 2016; 15(12): 1257-1272. [DOI]
5. Hirsch L, Jette N, Frolkis A, et al. The Incidence of Parkinson's Disease: A Systematic Review and Meta-Analysis. Neuroepidemiology 2016; 46(4): 292-300. [DOI]
6. Heidari N, Heidari P, Salari N, et al. A systematic re-view on risk factors and protective factors related to Parkinson's disease. Tehran Univ Med J 2022; 79(12): 925-933. [Article]
7. Trinh J, Zeldenrust FMJ, Huang J, et al. Genotype-phenotype relations for the Parkinson's disease genes SNCA, LRRK2, VPS35: MDSGene systematic review. Mov Disord 2018; 33(12): 1857-1870. [DOI]
8. Goldman SM. Environmental toxins and Parkinson's disease. Annu Rev Pharmacol Toxicol 2014; 54: 141-164. [DOI]
9. Schapira AHV, Jenner P. Etiology and pathogenesis of Parkinson's disease. Mov Disord 2011; 26(6): 1049-1055. [DOI]
10. Dias V, Junn E, Mouradian MM. The role of oxidative stress in Parkinson's disease. J Parkinsons Dis 2013; 3(4): 461-491. [DOI]
11. Tansey MG, Goldberg MS. Neuroinflammation in Parkinson's disease: its role in neuronal death and implications for therapeutic intervention. Neurobiol Dis 2010; 37(3): 510-518. [DOI]
12. Cheng HC, Ulane CM, Burke RE. Clinical progression in Parkinson disease and the neurobiology of axons. Ann Neurol 2010; 67(6): 715-725. [DOI]
13. Stoker TB, Greenland JC, editors. Parkinson's disease: pathogenesis and clinical aspects. Brisbane: Codon Publications; 2018. [DOI]
14. Huang X, Auinger P, Eberly S, et al. Serum cholesterol and the progression of Parkinson's disease: results from DATATOP. PLoS One 2011; 6(8): e22854. [DOI]
15. Qiang JK, Wong YC, Siderowf A, et al. Plasma apolipoprotein A1 as a biomarker for Parkinson dis-ease. Ann Neurol 2013; 74(1): 119-127. [DOI]
16. Hu G, Antikainen R, Jousilahti P, et al. Total cholesterol and the risk of Parkinson disease. Neurology 2008; 70(21): 1972-1979. [DOI]
17. Huang X, Chen H, Miller WC, et al. Lower low-density lipoprotein cholesterol levels are associated with Parkinson's disease. Mov Disord 2007; 22(3): 377-381. [DOI]
18. Blandini F, Armentero MT. Animal models of Park-inson's disease. FEBS J 2012; 279(7): 1156-1166. [DOI]
19. Iancu R, Mohapel P, Brundin P, et al. Behavioral characterization of a unilateral6- 6-OHDA-lesion model of Parkinson's disease in mice. Behav Brain Res 2005; 162(1): 1-10. [DOI]
20. Esmaeli MH, Haghdoost-Yazdi H, Mazaheri M. Increased serum lithium level due to mild to moderate damage to dopaminergic neurons of the substantia nigra: evidence from animal model of Parkinson's disease induced by 6-hydroxydopamine. SJKU 2022; 27(5): 10-23. (Persian) [DOI]
21. Badawi GA, Abd El Fattah MA, Zaki HF, et al. Sitagliptin and liraglutide reversed nigrostriatal degeneration of rodent brain in rotenone-induced Parkinson's disease. Inflammopharmacology 2017; 25(3): 369-382. [DOI]
22. Haghdoost Yazdi H, Sofiabadi M, Esmaeili MH, et al. Evaluation of the association between serum iron level and 6-hydroxydopamine-induced Parkinsonism in rats. Knowledge and Health in Basic Medical Sciences 2025; 19(4): 41-48. (Persian) [DOI]
23. Andereggen L, Meyer M, Guzman R, et al. Effects of GDNF pretreatment on function and survival of transplanted fetal ventral mesencephalic cells in the6-6-OHDA rat model of Parkinson's disease. Brain Res 2009; 1276: 39-49. [DOI]
24. Lin KC, Okamura H, Mori T. Inhibition of human chorionic gonadotropin-induced ovulation and steroido-genesis by shortterm hyperprolactinemia in female rabbits. Endocrinol Jpn 1987; 34(5): 675-683. [DOI]
25. Hong X, Guo W, Liu H, et al. Lower Blood Lipid Level Is Associated with the Occurrence of Parkinson's Disease: A Meta-Analysis and Systematic Review. Int J Clin Pract 2022; 2022: 9773038. [DOI]
26. Qiu J, Peng G, Tang Y, et al. Lipid profiles in the cerebrospinal fluid of rats with 6 hydroxydopamine induced lesions as a model of Parkinson’s disease. Front Aging Neurosci 2023; 14: 1077738. [DOI]
27. Luo S, Ezrokhi M, Cominos N, et al. Experimental dopaminergic neuron lesion at the area of the biological clock pacemaker, suprachiasmatic nuclei (SCN) induces metabolic syndrome in rats. Diabetol Metab Syndr 2021; 13(1): 11. [DOI]
28. Bustelli IB, Oliveira LM, CorreaNetto NF, et al. Behavioral effects of 6-hydroxydopamine-induced damage to nigrostriatal pathway and Locus coeruleus as a rodent model of Parkinson's disease. Behav Brain Res 2024; 462: 114873. [DOI]
29. Li Z, Zheng L, Wang J, et al. Dopamine in the regulation of glucose and lipid metabolism: a narrative review. Obesity (Silver Spring) 2024; 32(9): 1632-1645. [DOI]
30. Ozsoy O, Yildirim FB, Ogut E, et al. Melatonin is protective against 6-hydroxydopamine-induced oxidative stress in a hemiparkinsonian rat model. Free Radical Research 2015; 49(8): 1004–1014. [DOI]
31. Reichert CO, Levy D, Bydlowski SP. Paraoxonase Role in Human Neurodegenerative Diseases. Anti-oxidants (Basel) 2020; 10(1): 11. [DOI]
32. Cui J, Zhao D, Xu M, et al. Characterization of graded 6-Hydroxydopamine unilateral lesion in medial forebrain bundle of mice. Sci Rep 2024; 14(1): 3721. [DOI]
Send email to the article author
| Rights and Permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
