Brain kinin B1 receptor is upregulated by the oxidative stress and its activation leads to stereotypic nociceptive behavior in insulin-resistant rats

Dias, Jenny Pena; Gariepy, H. De Brito; Ongali, Brice; Couture, Réjean

doi:10.1016/j.peptides.2015.04.022

Cited by 11 publications

(13 citation statements)

References 47 publications

(89 reference statements)

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“…Although still not fully elucidated the molecular mechanism triggered by decreasing of ovarian hormones on the pain process and major depression. Clinical and preclinical data suggest that the decrease of ovarian hormones induce: (I) alteration of angiotensin-converting enzyme (ACE) activity, (II) increase of oxidative stress, and (III) increase of pro-inflammatory cytokines [45][46][47], which leads to increased production of kinin and receptors activation [40,48].…”

Section: Discussionmentioning

confidence: 99%

“…The reduction of estrogen levels has been associated with increased reactive oxygen species (ROS) [50][51][52]. In preclinical studies, the increase of ROS induced upregulation of B1R on the rat brain submitted to the insulin resistance model [47]. The increase of B1R activity leads to downstream pathways involving an increase of nitric oxide (NO), glutamate, and substance P (SP) [47].…”

Section: Discussionmentioning

confidence: 99%

“…In preclinical studies, the increase of ROS induced upregulation of B1R on the rat brain submitted to the insulin resistance model [47]. The increase of B1R activity leads to downstream pathways involving an increase of nitric oxide (NO), glutamate, and substance P (SP) [47]. Also, ovariectomized mice showed an increase of nitric oxide (NO) in the hippocampus, and the acute treatment with non-selective NO synthase inhibitor (L-NAME) significantly decreases the immobility time of OVX mice in the FST [17].…”

Section: Discussionmentioning

confidence: 99%

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Blockade of Kinin B₁receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Maciel

Azevedo

Oliboni

et al. 2020

Preprint

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Menopause is related to a decline in ovarian estrogen production, affecting the perception of the somatosensory stimulus, changing the immune-inflammatory systems, and triggering depressive symptoms. Inhibition of kinin B1 and B2 receptors (B1R and B2R) inhibits the depressive-like behavior and mechanical allodynia induced by immune-inflammatory mediators in mice. However, there is no evidence on the role of kinin receptors in depressive-like and nociceptive behavior in female mice submitted to bilateral ovariectomy. This study shows that ovariectomized mice (OVX) developed time-related mechanical allodynia and increased immobility time in the tail suspension test (TST). The genetic deletion of B1R, or the pharmacological blockade by selective kinin B1R antagonist R-715 (acute, i.p), reduced the increase of immobility time and mechanical allodynia induced by ovariectomy. Neither genetic deletion nor pharmacological inhibition of B2R (HOE 140, i.p) prevented the behavioral changes elicited by OVX. Our data suggested a particular modulation of kinin B1R in the nociceptive and depressive-like behavior in ovariectomized mice. Selective inhibition of the B1R receptor may be a new pharmacological target for treating pain and depression symptoms in women on the perimenopause/menopause period.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Blockade of Kinin B₁receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Maciel

Azevedo

Oliboni

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…1,18,34 A study using bradykinin receptor-null mice indicated that nonselective stimulation of B 1 R and B 2 R is likely to suppress oxidative stress and diabetic nephropathy, 23 while other studies suggested that the selective activation of B 2 R 25 and inhibition of B 1 R could be beneficial. 27,46 Data from studies on the vascular system of diabetic rats showed that B 1 R enhances superoxide anion radical formation by activating NADPH oxidase. 18,27,46 Moreover, it has been shown that oxidative stress caused by elevated superoxide anion production induces expression of the kinin B 1 R in the liver and brain of diabetic rats.…”

Section: What's New?mentioning

confidence: 99%

“…27,46 Data from studies on the vascular system of diabetic rats showed that B 1 R enhances superoxide anion radical formation by activating NADPH oxidase. 18,27,46 Moreover, it has been shown that oxidative stress caused by elevated superoxide anion production induces expression of the kinin B 1 R in the liver and brain of diabetic rats. [46][47][48] In light of recent findings, the cooperation between G protein-coupled receptors makes the signal transduction pathways of active peptides even more complex.…”

Section: What's New?mentioning

confidence: 99%

Bradykinin and oxidative stress in patients with hereditary angioedema due to C1 inhibitor deficiency

Obtułowicz¹,

Góralska²,

Bogdali-Suślik³

et al. 2020

Polish Archives of Internal Medicine

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INTROduCTION Hereditary angioedema (HAE) is a rare autosomal dominant disease caused by genetic dysfunction of C1 inhibitor (C1-INH) due to mutations in the SERPING1 gene. The disorder is mediated mainly by bradykinin. The clinical course of the disease is varied and not related to genetic changes. OBjECTIvEs We aimed to evaluate redox homeostasis of peripheral blood mononuclear cells (PBMCs) in patients with HAE due to C1-INH deficiency (C1-INH-HAE) by measuring the levels of reactive oxygen species (ROS) of PBMCs as well as plasma advanced glycation end products (AGEs) and advanced oxidation protein products (AOPPs). We also aimed to assess the effect of bradykinin on ROS levels. PATIENTs ANd mEThOds We enrolled 30 adults with C1-INH-HAE and 15 healthy individuals. The levels of ROS were measured by flow cytometry, while the plasma levels of AGEs and AOPPs were determined spectrophotometrically by enzyme-linked immunosorbent assays. REsuLTs Basal and hydrogen peroxide (H 2 O 2)-induced ROS levels were higher in patients with HAE when compared with controls (P = 0.002 and P = 0.001, respectively), indicating abnormalities in redox homeostasis. Plasma AOPP and AGE levels were similar in both groups. Bradykinin reduced basal and H 2 O 2-induced ROS generation in PBMCs only in patients with HAE (P = 0.03). CONCLusIONs The higher basal and H 2 O 2-induced ROS levels in patients with C1-INH-HAE indicate redox imbalance. However, by reducing basal and H 2 O 2-induced ROS levels, bradykinin shows antioxidant action in this disorder.

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Primary Role for Kinin B1 and B2 Receptors in Glioma Proliferation

et al. 2016

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This study investigated the role of kinins and their receptors in malignant brain tumors. As a first approach, GL-261 glioma cells were injected (2 × 10 cells in 2 μl/2 min) into the right striatum of adult C57/BL6 wild-type, kinin B and B receptor knockout (KOBR and KOBR) and B and B receptor double knockout mice (KOBBR). The animals received the selective BR (SSR240612) and/or BR (HOE-140) antagonists by intracerebroventricular (i.c.v.) route at 5, 10, and 15 days. The tumor size quantification, mitotic index, western blot analysis, quantitative autoradiography, immunofluorescence, and confocal microscopy were carried out in brain tumor samples, 20 days after tumor induction. Our results revealed an uncontrolled tumor growing in KOBR or SSR240612-treated mice, which was blunted by BR blockade with HOE-140, suggesting a crosstalk between BR and BR in tumor growing. Combined treatment with BR and BR antagonists normalized the upregulation of tumor BR and decreased the tumor size and the mitotic index, as was seen in double KOBBR. The BR was detected on astrocytes in the tumor, indicating a close relationship between this receptor and astroglial cells. Noteworthy, an immunohistochemistry analysis of tumor samples from 16 patients with glioma diagnosis revealed a marked BR immunopositivity in low-grade gliomas or in older glioblastoma individuals. Furthermore, the clinical data revealed a significantly higher immunopositivity for BR, when compared to a lower BR immunolabeling. Taken together, our results show that blocking simultaneously both kinin receptors or alternatively stimulating BR may be of therapeutic value in the treatment of brain glioblastoma growth and malignancy.

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Brain kinin B1 receptor is upregulated by the oxidative stress and its activation leads to stereotypic nociceptive behavior in insulin-resistant rats

Cited by 11 publications

References 47 publications

Blockade of Kinin B₁receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Blockade of Kinin B₁receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Bradykinin and oxidative stress in patients with hereditary angioedema due to C1 inhibitor deficiency

Primary Role for Kinin B1 and B2 Receptors in Glioma Proliferation

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Brain kinin B1 receptor is upregulated by the oxidative stress and its activation leads to stereotypic nociceptive behavior in insulin-resistant rats

Cited by 11 publications

References 47 publications

Blockade of Kinin B1receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Blockade of Kinin B1receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Bradykinin and oxidative stress in patients with hereditary angioedema due to C1 inhibitor deficiency

Primary Role for Kinin B1 and B2 Receptors in Glioma Proliferation

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Blockade of Kinin B₁receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Blockade of Kinin B₁receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice