Histamine ameliorates anti-glomerular basement membrane antibody-induced glomerulonephritis in rats

Tanda, S.; Mori, Yoshihide; Kimura, Takayasu; Sonomura, Kazuhiro; Kusaba, Tetsuro; Kishimoto, Noriko; Kameyama, Hisako; Tamagaki, Keiichi; Okigaki, Mitsuhiko; Hatta, Tsuguru; Sasaki, Susumu; Takeda, Kyoichi; Sado, Yoshikazu; Adachi, Naoto; Matsubara, Hiroki

doi:10.1038/sj.ki.5002370

Cited by 13 publications

(10 citation statements)

References 31 publications

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“…Other possible mechanisms associated with initial FcR activation by anti-GBM antibody, such as acute cytokine activation or production of reactive oxygen species in glomeruli and subsequent tubular damage, 27,28 could play an additional role.…”

Section: Discussionmentioning

confidence: 99%

Peritubular Ischemia Contributes More to Tubular Damage than Proteinuria in Immune-Mediated Glomerulonephritis

Suzuki¹,

Tanifuji²,

Akiba³

et al. 2008

Journal of the American Society of Nephrology

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Proteinuria is a key factor in the progression of tubulointerstitial injury. Recently, tubular ischemia as a result of loss of peritubular capillaries has been identified as another major contributor to disease progression, but the relative contribution of these insults on tubulointerstitial damage is unknown. Anti-glomerular basement membrane glomerulonephritis was induced in wild-type (WT) and Fc receptor knockout (FcRKO) mice, which have been shown to be relatively protected against glomerular endothelial injury. Despite comparable degrees of proteinuria, WT mice developed significantly worse renal function than FcRKO mice, along with higher expression of both type I collagen and kidney injury molecule-1 (a sensitive marker of acute tubular injury) by real-time PCR and immunohistochemistry. In addition, compared with FcRKO mice, WT mice exhibited a greater decrease in peritubular red blood cell velocity by intravital videomicroscopy and a marked increase of tissue hypoxia. In vitro, kidney injury molecule-1 expression increased in cultured mouse proximal tubular epithelial cells in response to cellular stresses, including hypoxia, starvation, and exposure to excessive protein; therefore, it is suggested that hypoxic insults more strongly influence tubulointerstitial damage than proteinuria alone in models of subacute renal disease.

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Section: Discussionmentioning

confidence: 99%

Peritubular Ischemia Contributes More to Tubular Damage than Proteinuria in Immune-Mediated Glomerulonephritis

Suzuki¹,

Tanifuji²,

Akiba³

et al. 2008

Journal of the American Society of Nephrology

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“…The histaminergic receptors in the hypothalamus appear to be an important mediator of feeding behavior and body weight regulation [20], which may further regulate obesity and dyslipidemia [21,22]. The high binding affinity of SGAs to H1R and its modulating role in the hypothalamic AMPK pathway have been evidenced as one key mechanism for a marked increase in food-intake/weight gain [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Betahistine co-treatment ameliorates dyslipidemia induced by chronic olanzapine treatment in rats through modulation of hepatic AMPKα-SREBP-1 and PPARα-dependent pathways

Liu¹,

Lian

et al. 2015

Pharmacological Research

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Second-generation antipsychotics including olanzapine are associated with weight gain, dyslipidemia and other metabolic disorders. Both animal and clinical studies have shown that co-treatment with betahistine (a histamine H1 receptor agonist/H3 receptor antagonist) is effective in controlling olanzapine-induced weight gain. In the present study, we investigate whether co-treatment with betahistine is able to prevent dyslipidemia induced by chronic olanzapine treatment and the underlying mechanisms. Female rats were orally administered with olanzapine (1 mg/kg, t.i.d.) for 3.5 consecutive weeks and then a 2.5-week drug withdrawal. Then, rats were divided into 4 groups for 5 weeks treatment: (1) vehicle, (2) olanzapine-only (1 mg/kg, t.i.d.), (3) betahistine-only (9.6 mg/kg, t.i.d.), and (4) olanzapine and betahistine (O+B) co-treatment. After completing treatment, hepatic mRNA expression was measured by qRT-PCR, while the protein levels were detected by western blot. In our study, olanzapine-only treatment significantly increased triglyceride accumulation and non-esterified fatty acids (NEFA), and upregulated mRNA expression of sterol regulatory element binding protein 1 (SREBP-1) and its target genes, while these alterations were ameliorated by O+B co-treatment. Hepatic AMP-activated protein kinase α (AMPKα) was activated in the O+B co-treatment group, with a significant reduction in nuclear SREBP-1 protein expression but an increased expression of peroxisome proliferator-activated receptor-α (PPARα) and its-responsive molecule(CPT1A), compared with olanzapine-only treatment. In addition, olanzapine significantly increased hepatic histamine H1 receptors, while O+B co-treatment significantly reversed them to normal levels. This study provided the first evidence that betahistine could act on hepatic H1 receptors via modulation of AMPKα-SREBP-1 and PPARα-dependent pathways to ameliorate olanzapine-induced dyslipidemia in rats.

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“…In this Th1-driven, DTH-mediated model, histamine reduced the expression of the Th1-inducing cytokine IL-12. 126 …”

Section: Role Of Mast Cells In Inflammatory and Autoimmune Kidney Dismentioning

confidence: 99%

Role of Mast Cells in Progressive Renal Diseases

Holdsworth¹,

Summers²

2008

Journal of the American Society of Nephrology

119

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Histamine ameliorates anti-glomerular basement membrane antibody-induced glomerulonephritis in rats

Cited by 13 publications

References 31 publications

Peritubular Ischemia Contributes More to Tubular Damage than Proteinuria in Immune-Mediated Glomerulonephritis

Peritubular Ischemia Contributes More to Tubular Damage than Proteinuria in Immune-Mediated Glomerulonephritis

Betahistine co-treatment ameliorates dyslipidemia induced by chronic olanzapine treatment in rats through modulation of hepatic AMPKα-SREBP-1 and PPARα-dependent pathways

Role of Mast Cells in Progressive Renal Diseases

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