Effects of D-allose on OGD/R-induced HT22 cell damage and Gal-3 expression

doi:10.3877/cma.j.issn.2095-9141.2023.03.002

Abstract

Abstract:

Objective

To investigate the effects of D-allose treatment on oxygen glucose deprivation/reperfusion (OGD/R) induced HT22 cell damage and galactin-3 (Gal-3) expression.

Methods

HT22 cells in normal culture were randomly divided into control group, OGD/R group, D-allose group and inhibitor group after passage and adhesion. OGD/R model was constructed and set it as the OGD/R group. D-allose group: OGD/R model was constructed, 10 mmol/L D-allose was added into the medium during the reoxygenation and reglucose and continued until the end of the reoxygenation and reglucose. Inhibitor group: OGD/R model was constructed, and D-allose and TD139 were added to the culture medium at the same time during reoxygenation and disaccharide, which lasted until the end of reoxygenation and disaccharide. CCK8 assay was used to detect cell survival rate. The expression of Gal-3 and apoptosis-related proteins Bax, Bcl-2, Caspase-3, Cleaved caspase-3 were detected by Western blot. Apoptosis was detected by flow cytometry.

Results

Compared with OGD/R group, the survival rate of cells in D-allose group was significantly increased, the apoptosis rate was significantly decreased, the protein expression levels of Bax, Cleaved caspase-3, Gal-3 and LGALS3BP were significantly decreased, and the expression level of Bcl-2 protein was significantly increased, with statistical significance (P<0.05); but there was no significant difference in Caspase-3 protein expression (P>0.05). Compared with the D-allose group, the expression of Bcl-2/Bax in inhibitor group was significantly increased, Cleaved caspase-3 protein expression was significantly decreased, with statistical significance (P<0.05); there was no significant difference in Caspase-3 protein expression (P>0.05).

Conclusion

D-allose treatment has a protective effect on OGD/R-induced HT22 cell damage, and D-allose may play a protective role by inhibiting Gal-3.

Key words: HT22 cell, Oxygen glucose deprivation/reperfusion, D-allose, Galactin-3

Min Zhang, Xiaowei Fei, Yaowen Luo, Yihao Fu, Lei Zhang, Dakuan Gao. Effects of D-allose on OGD/R-induced HT22 cell damage and Gal-3 expression[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2023, 09(03): 135-141.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhsjcswkdzzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.2095-9141.2023.03.002

https://zhsjcswkdzzz.cma-cmc.com.cn/EN/Y2023/V09/I03/135

Figures/Tables 7

Fig.1 Effects of OGD/R processing time on the survival rate of HT22 cells (n=6)

Fig.2 Effects of OGD/R processing time on Gal-3 protein expression in HT22 cells (n=3)

Fig.3 Effect of different concentrations of D-allose on cell survival after OGD/R (n=6)

Fig.4 Effect of D-allose on apoptosis after OGD/R (n=3)

Fig.5 Effect of D-allose on apoptosis-related protein expression after OGD/R (n=3)

Fig.6 Effect of D-allose on expression of Gal-3 and downstream protein after OGD/R (n=3)

Fig.7 Effect of TD139 on apoptosis-related protein expression after OGD/R (n=3)

References 23

[1]	周良辅.砥砺前行——试论我国脑卒中的防治[J].中华脑科疾病与康复杂志(电子版), 2021, 11: 1-3. DOI: 10.3877/cma.j.issn.2095-123X.2021.01.001.
[2]	王亚楠,吴思缈,刘鸣.中国脑卒中15年变化趋势和特点[J].华西医学, 2021, 36(6): 803-807. DOI: 10.7507/1002-0179.202105046.
[3]	Wu M, Gu X, Ma Z. Mitochondrial quality control in cerebral ischemia-reperfusion injury[J]. Mol Neurobiol, 2021, 58(10): 5253-5271. DOI: 10.1007/s12035-021-02494-8.
[4]	Kishida K, Iida T, Yamada T, et al. d-Allose is absorbed via sodium-dependent glucose cotransporter 1 (SGLT1) in the rat small intestine[J]. Metabol Open, 2021, 11: 100112. DOI: 10.1016/j.metop.2021.100112.
[5]	Khajeh S, Ganjavi M, Panahi G, et al. D-allose: molecular pathways and therapeutic capacity in cancer[J]. Curr Mol Pharmacol, 2023, 16(8): 801-810. DOI: 10.2174/1874467216666221227105011.
[6]	Sui L, Nomura R, Dong Y, et al. Cryoprotective effects of D-allose on mammalian cells[J]. Cryobiology, 2007, 55(2): 87-92. DOI: 10.1016/j.cryobiol.2007.05.003.
[7]	Blanda V, Bracale UM, Di Taranto MD, et al. Galectin-3 in cardiovascular diseases[J]. Int J Mol Sci, 2020, 21(23): 9232. DOI: 10.3390/ijms21239232.
[8]	Ekingen E, Yilmaz M, Yildiz M, et al. Utilization of glial fibrillary acidic protein and galectin-3 in the diagnosis of cerebral infarction patients with normal cranial tomography[J]. Niger J Clin Pract, 2017, 20(4): 433-437. DOI: 10.4103/1119-3077.187311.
[9]	Jagodzinski A, Havulinna AS, Appelbaum S, et al. Predictive value of galectin-3 for incident cardiovascular disease and heart failure in the population-based FINRISK 1997 cohort[J]. Int J Cardiol, 2015, 192: 33-39. DOI: 10.1016/j.ijcard.2015.05.040.
[10]	张永康,韩燕.半乳糖凝集素-3与脑卒中：从病理生理学到临床的研究进展[J].安徽医药, 2022, 26(3): 434-438. DOI: 10.3969/j.issn.1009-6469.2022.03.003.
[11]	Doverhag C, Hedtjärn M, Poirier F, et al. Galectin-3 contributes to neonatal hypoxic-ischemic brain injury[J]. Neurobiol Dis, 2010, 38(1): 36-46. DOI: 10.1016/j.nbd.2009.12.024.
[12]	Cui Y, Zhang NN, Wang D, et al. Modified citrus pectin alleviates cerebral ischemia/reperfusion injury by inhibiting NLRP3 inflammasome activation via TLR4/NF-κB signaling pathway in microglia[J]. J Inflamm Res, 2022, 15: 3369-3385. DOI: 10.2147/jir.S366927.
[13]	马甜甜.半乳糖凝集素-3对脑卒中后认知功能障碍的预测作用研究进展[J].现代医药卫生, 2022, 38(23): 4075-4078. DOI: 10.3969/j.issn.1009-5519.2022.23.025.
[14]	Gao D, Kawai N, Tamiya T. The anti-inflammatory effects of D-allose contribute to attenuation of cerebral ischemia-reperfusion injury[J]. Med Hypotheses, 2011, 76(6): 911-913. DOI: 10.1016/j.mehy.2011.03.007.
[15]	Gao D, Kawai N, Nakamura T, et al. Anti-inflammatory effect of D-allose in cerebral ischemia/reperfusion injury in rats[J]. Neurol Med Chir (Tokyo), 2013, 53(6): 365-374. DOI: 10.2176/nmc.53.365.
[16]	Huang T, Gao D, Hei Y, et al. D-allose protects the blood brain barrier through PPARγ-mediated anti-inflammatory pathway in the mice model of ischemia reperfusion injury[J]. Brain Res, 2016, 1642: 478-486. DOI: 10.1016/j.brainres.2016.04.038.
[17]	Zhang M, Fu YH, Luo YW, et al. d-allose protects brain microvascular endothelial cells from hypoxic/reoxygenated injury by inhibiting endoplasmic reticulum stress[J]. Neurosci Lett, 2023, 793: 137000. DOI: 10.1016/j.neulet.2022.137000.
[18]	Zhang L, Huang Y, Lou H, et al. LGALS3BP/Gal-3 promotes osteogenic differentiation of human periodontal ligament stem cells[J]. Arch Oral Biol, 2021, 128: 105149. DOI: 10.1016/j.archoralbio.2021.105149.
[19]	He XW, Li WL, Li C, et al. Serum levels of galectin-1, galectin-3, and galectin-9 are associated with large artery atherosclerotic stroke[J]. Sci Rep, 2017, 7: 40994. DOI: 10.1038/srep40994.
[20]	Cibor D, Szczeklik K, Brzozowski B, et al. Serum galectin 3, galectin 9 and galectin 3-binding proteins in patients with active and inactive inflammatory bowel disease[J]. J Physiol Pharmacol, 2019, 70(1). DOI: 10.26402/jpp.2019.1.06.
[21]	Harazono Y, Nakajima K, Raz A. Why anti-Bcl-2 clinical trials fail: a solution[J]. Cancer Metastasis Rev, 2014, 33(1): 285-294. DOI: 10.1007/s10555-013-9450-8.
[22]	Hirani N, Mackinnon AC, Nicol L, et al. Target inhibition of galectin-3 by inhaled TD139 in patients with idiopathic pulmonary fibrosis[J]. Eur Respir J, 2021, 57(5): 2002559. DOI: 10.1183/13993003.02559-2020.
[23]	Li H, Xiao L, He H, et al. Quercetin Attenuates Atherosclerotic Inflammation by Inhibiting Galectin-3-NLRP3 Signaling Pathway[J]. Mol Nutr Food Res, 2021, 65(15): e2000746. DOI: 10.1002/mnfr.202000746.

Please choose a citation manager

Content to export