1,25-dihydroxyvitamin D3 ameliorates lupus nephritis through inhibiting the NF-κB and MAPK signalling pathways in MRL/lpr mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2022-07-08

AUTHORS

Xuewei Li, Jie Liu, Yingzhe Zhao, Ning Xu, E. Lv, Chunzeng Ci, Xiangling Li

ABSTRACT

BackgroundLupus nephritis (LN) is a common and serious complication of systemic lupus erythematosus (SLE). However, the aetiology and pathogenesis of LN remain unknown. 1,25-dihydroxyvitamin D3 [1,25-(OH)2-VitD3] is the active form of vitamin D, and it has been shown to perform important functions in inflammatory and immune-related diseases. In this study, we investigated the time-dependent effects of 1,25-dihydroxyvitamin D3 and explored the underlying mechanism in MRL/lpr mice, a well-studied animal model of LN.MethodsBeginning at 8 weeks of age, 24-h urine samples were collected weekly to measure the levels of protein in the urine. We treated female MRL/lpr mice with 1,25-dihydroxyvitamin D3 (4 μg/kg) or 1% DMSO by intraperitoneal injection twice weekly for 3 weeks beginning at the age of 11 weeks. The mice were separately sacrificed, and serum and kidney samples were collected at the ages of 14, 16, 18, and 20 weeks to measure creatinine (Cr) levels, blood urea nitrogen (BUN) levels, histological damage, immunological marker (A-ds DNA, C1q, C3, IgG, IgM) levels, and inflammatory factor (TNF-α, IL-17, MCP-1) levels. Furthermore, the nuclear factor kappa B (NF-κB) and the mitogen-activated protein kinase (MAPK) signalling pathways were also assessed to elucidate the underlying mechanism.ResultsWe found that MRL/lpr mice treated with 1,25-dihydroxyvitamin D3 displayed significantly attenuated LN. VitD3-treated mice exhibited significantly improved renal pathological damage and reduced proteinuria, BUN, SCr, A-ds DNA antibody and immune complex deposition levels (P < 0.05) compared with untreated MRL/lpr mice. Moreover, 1,25-dihydroxyvitamin D3 inhibited the complement cascade, inhibited the release of proinflammatory cytokines, such as TNF-α, IL-17, and MCP-1, and inhibited NF-κB and MAPK activation (P < 0.05).Conclusion1,25-dihydroxyvitamin D3 exerts a protective effect against LN by inhibiting the NF-κB and MAPK signalling pathways, providing a potential treatment strategy for LN. Interestingly, the NF-κB and MAPK signalling pathways are time-dependent mediators of LN and may be associated with lupus activity. More... »

PAGES

243

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12882-022-02870-z

DOI

http://dx.doi.org/10.1186/s12882-022-02870-z

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https://app.dimensions.ai/details/publication/pub.1149341345

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/35804318


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31 schema:description BackgroundLupus nephritis (LN) is a common and serious complication of systemic lupus erythematosus (SLE). However, the aetiology and pathogenesis of LN remain unknown. 1,25-dihydroxyvitamin D3 [1,25-(OH)2-VitD3] is the active form of vitamin D, and it has been shown to perform important functions in inflammatory and immune-related diseases. In this study, we investigated the time-dependent effects of 1,25-dihydroxyvitamin D3 and explored the underlying mechanism in MRL/lpr mice, a well-studied animal model of LN.MethodsBeginning at 8 weeks of age, 24-h urine samples were collected weekly to measure the levels of protein in the urine. We treated female MRL/lpr mice with 1,25-dihydroxyvitamin D3 (4 μg/kg) or 1% DMSO by intraperitoneal injection twice weekly for 3 weeks beginning at the age of 11 weeks. The mice were separately sacrificed, and serum and kidney samples were collected at the ages of 14, 16, 18, and 20 weeks to measure creatinine (Cr) levels, blood urea nitrogen (BUN) levels, histological damage, immunological marker (A-ds DNA, C1q, C3, IgG, IgM) levels, and inflammatory factor (TNF-α, IL-17, MCP-1) levels. Furthermore, the nuclear factor kappa B (NF-κB) and the mitogen-activated protein kinase (MAPK) signalling pathways were also assessed to elucidate the underlying mechanism.ResultsWe found that MRL/lpr mice treated with 1,25-dihydroxyvitamin D3 displayed significantly attenuated LN. VitD3-treated mice exhibited significantly improved renal pathological damage and reduced proteinuria, BUN, SCr, A-ds DNA antibody and immune complex deposition levels (P < 0.05) compared with untreated MRL/lpr mice. Moreover, 1,25-dihydroxyvitamin D3 inhibited the complement cascade, inhibited the release of proinflammatory cytokines, such as TNF-α, IL-17, and MCP-1, and inhibited NF-κB and MAPK activation (P < 0.05).Conclusion1,25-dihydroxyvitamin D3 exerts a protective effect against LN by inhibiting the NF-κB and MAPK signalling pathways, providing a potential treatment strategy for LN. Interestingly, the NF-κB and MAPK signalling pathways are time-dependent mediators of LN and may be associated with lupus activity.
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38 BackgroundLupus nephritis
39 D3
40 DMSO
41 DNA antibodies
42 IL-17
43 Ln
44 MAPK activation
45 MAPK signaling pathways
46 MCP-1
47 MRL/lpr mice
48 NF-κB
49 ResultsWe
50 SCR
51 TNF
52 VitD3
53 activation
54 active form
55 activity
56 age
57 animal models
58 antibodies
59 blood urea nitrogen levels
60 cascade
61 complement cascade
62 complications
63 creatinine levels
64 cytokines
65 damage
66 deposition levels
67 dihydroxyvitamin D3
68 disease
69 effect
70 erythematosus
71 etiology
72 factor kappa B
73 factor levels
74 female MRL/lpr mice
75 form
76 function
77 histological damage
78 immune-related diseases
79 important functions
80 inflammatory factor levels
81 injection
82 intraperitoneal injection
83 kappa B
84 kidney samples
85 kinase
86 levels
87 levels of protein
88 lpr mice
89 lupus
90 lupus activity
91 lupus erythematosus
92 marker levels
93 mechanism
94 mediators
95 mice
96 mitogen-activated protein kinase
97 model
98 nephritis
99 nitrogen levels
100 nuclear factor kappa B
101 pathogenesis
102 pathogenesis of LN
103 pathological damage
104 pathway
105 potential treatment strategy
106 proinflammatory cytokines
107 protective effect
108 protein
109 protein kinase
110 proteinuria
111 release
112 renal pathological damage
113 samples
114 serious complications
115 serum
116 signaling pathways
117 strategies
118 study
119 systemic lupus erythematosus
120 time-dependent effects
121 time-dependent mediators
122 treatment strategies
123 underlying mechanism
124 untreated MRL/lpr mice
125 urea nitrogen levels
126 urine
127 urine samples
128 vitamin D
129 weeks
130 weeks of age
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