Exercise and complex environment inhibiting lipopolysaccharide-induced dopaminergic neuron damage in substantia nigra

CAO Cong HUANG Qin-wen WANG Hong XU Ze-ting ZHANG Chan3 SHAN Yi-wen FAN Xiao-xiao LIAO Min

Acta Anatomica Sinica ›› 2024, Vol. 55 ›› Issue (3) : 253-259.

PDF(2033 KB)
Welcome to visit Acta Anatomica Sinica! Today is Chinese
PDF(2033 KB)
Acta Anatomica Sinica ›› 2024, Vol. 55 ›› Issue (3) : 253-259. DOI: 10.16098/j.issn.0529-1356.2024.03.001
Neurobiology

Exercise and complex environment inhibiting lipopolysaccharide-induced dopaminergic neuron damage in substantia nigra

  • CAO  Cong1 HUANG Qin-wen2 WANG Hong2  XU Ze-ting2  ZHANG  Chan3  SHAN Yi-wen4  FAN Xiao-xiao2  LIAO Min2* 
Author information +
History +

Abstract

Objective   To investigate the effects of exercise and complex environment on lipopolysaccharide (LPS)-induced dopaminergic neuron death in the substantia nigra of midbrain.   Methods C57BL/6 mice were divided into control group, LPS group, LPS+swimming group and LPS+complex environment group, with 7 mice in each group. The mice in the LPS group were injected with LPS into the brain to establish an inflammatory model of Parkinson ’s disease and lived in cages for 2 weeks. Mice in LPS+swimming group were forced to swim for 15 minutes every day for 2 weeks after modeling. The mice in the LPS+complex environment group were placed in a complex environment for 2 weeks after modeling. The control group mice were not treated. After 14 days of modeling, behavioral experiments such as footprint, open field and rotating rod were performed on each group of mice to detect the autonomous exercise ability, exercise balance ability and depression level of mice. The expressions of tyrosine hydroxylase (TH) in substantia nigra was detected by immunohistochemical staining and Western blotting. The expressions of brain-derived neurotrophic factor (BDNF), Caspase-3, interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) in the substantia nigra of the midbrain were detected by Western blotting. The transcription levels of IL-1β, IL-6 and TNF-α in substantia nigra were detected by RT-PCR.   Results  Compared with the control group, the exercise ability and balance ability of mice in LPS group, LPS+swimming group and LPS+complex environment group decreased, the depression level increased(P<0.001), the number of TH positive neurons and BDNF protein decreased significantly(P<0.001), and the contents of Caspase-3, IL-1β, IL-6 and TNF-α increased significantly(P<0.001). Compared with the LPS group, the exercise ability and balance ability of the mice in the LPS+swimming group and the LPS+complex environment group were restored, the depression level decreased significantly(P<0.01), the survival number of TH positive neurons and the content of BDNF increased significantly(P<0.01), Caspase-3, IL-1β, IL-6 and TNF-α  reduced significantly(P<0.01), and the phenomenon in the LPS+complex environment group was more significant.   Conclusion Exercise and complex environment can inhibit LPS-induced central nervous system inflammation in mice, thereby reducing damage to midbrain substantia nigra neurons, and the inhibitory effect of LPS+complex environment group is more significant.

Key words

Movement
/ Complex environment / Inflammation / Dopaminergic neuron / Lipopolysaccharide / Behavioral experiment / Western blotting / Mouse

Cite this article

Download Citations
CAO Cong HUANG Qin-wen WANG Hong XU Ze-ting ZHANG Chan3 SHAN Yi-wen FAN Xiao-xiao LIAO Min. Exercise and complex environment inhibiting lipopolysaccharide-induced dopaminergic neuron damage in substantia nigra[J]. Acta Anatomica Sinica. 2024, 55(3): 253-259 https://doi.org/10.16098/j.issn.0529-1356.2024.03.001

References

[1] GBD 2016 Parkinson’s Disease Collaborators. Global, regional, and national burden of Parkinson’s disease, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016 [J]. Lancet Neurol, 2018, 17(11): 939-953.
[2] Weintraub D, Aarsland D, Chaudhuri KR, et al. The neuropsychiatry of Parkinson’s disease: advances and challenges [J]. Lancet Neurol, 2022, 21(1): 89-102.
[3] Tansey MG, Wallings RL, Houser MC, et al. Inflammation and immune dysfunction in Parkinson disease [J]. Nat Rev Immunol, 2022, 22(11): 657-673.
[4] Tian J, Kang Y, Liu P, et al. Effect of physical activity on depression in patients with Parkinson’s disease: a systematic review and meta-analysis [J]. 
Int J Environ Res Public Health, 2022, 19(11): 6849.
[5] Almikhlafi MA. The role of exercise in Parkinson’s disease [J]. Neurosciences, 2023, 28(1): 4-12.
[6] Piercy KL, Troiano RP, Ballard RM, et al. The physical activity guidelines for Americans [J]. JAMA, 2018, 320(19): 2020-2028.
[7] Di liegro CM, Schiera G, Proia P, et al. Physical activity and brain health [J]. Genes, 2019, 10(9): 720.
[8] Vaynman S, Ying Z, Gomez-Pinilla F. Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition [J]. Eur J Neurosci, 2004, 20(10): 2580-2590.
[9] Neeper SA, Gomez-Pinilla F, Choi J, et al. Exercise and brain neurotrophins [J]. Nature, 1995, 373(6510): 109.
[10] Liang J, Wang H, Zeng Y, et al. Physical exercise promotes brain remodeling by regulating epigenetics, neuroplasticity and neurotrophins [J]. Rev Neurosci, 2021, 32(6): 615-629.
[11] Ben-Zeev T, Shoenfeld Y, Hoffman JR. The effect of exercise on neurogenesis in the brain [J]. Isr Med Assoc J, 2022, 24(8): 533-538.
[12] Nicklas BJ, Brinkley TE. Exercise training as a treatment for chronic inflammation in the elderly [J]. Exerc Sport Sci Rev, 2009, 37(4): 165-170.
[13] Erekat N, Al-Jarrah MD. Interleukin-1 beta and tumor necrosis factor alpha upregulation and nuclear factor kappa b activation in skeletal muscle from a mouse model of chronic/progressive Parkinson disease [J]. Med Sci Moni, 2018, 24: 7524-7531.
[14] Deng I, Corrigan F, Zhai G, et al. Lipopolysaccharide animal models of Parkinson’s disease: recent progress and relevance to clinical disease [J]. Brain Behav Immun Health, 2020, 4: 100060.
[15] Garber CE, Blissmer B, Deschenes MR, et al. American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise [J]. Med Sci Sports Exerc, 2011, 43(7): 1334-1359.
[16] Li F, Harmer P, Fitzgerald K, et al. Tai chi and postural stability in patients with Parkinson’s disease [J]. N Engl J Med, 2012, 366(6): 511-519.
[17] Bouca-Machado R, Venturelli M, Tinazzi M, et al. Treating patients like athletes: sports science applied to Parkinson’s disease [J]. Front Neurol, 2020, 11: 228.
[18] Bastioli G, Arnold JC, Mancini M, et al. Voluntary exercise boosts striatal dopamine release: evidence for the necessary and sufficient role of BDNF [J]. J Neurosci, 2022, 42(23): 4725-4736.
[19] Kallies G, Rapp MA, Fydrich T, et al. Serum brain-derived neurotrophic factor (BDNF) at rest and after acute aerobic exercise in major depressive disorder [J]. Psychoneuroendocrinology, 2019, 102: 212-215.

[20] Li W, Zhou X, Xie ZhY, et al. Voluntary wheel running prevents the formaldehyde induced negative emotion through up-regulation of hippocampal neurogenesis in mice [J]. Acta Anatomica Sinica, 2021, 52(5): 686-691.(in Chinese)

李威, 周鑫, 谢志艳,等. 自主跑轮运动通过促进海马神经发生改善甲醛所致小鼠的负性情绪 [J]. 解剖学报, 2021, 52(5): 686-691.
[21] Nay K, Smiles WJ, Kaiser J, et al. Molecular mechanisms underlying the beneficial effects of exercise on brain function and neurological disorders [J]. Int J Mol Sci, 2021, 22(8): 4052.

PDF(2033 KB)

Accesses

Citation

Detail

Sections
Recommended

/