Effects of neferine on CCL5 and CCR5 expression in SCG of type 2 diabetic rats

Li, Guilin; Xu, Hong; Zhu, Shuanghua; Xu, Wenyuan; Qin, Shu-Lan; Liu, Shuangmei; Tu, Guihua; Peng, Haiying; Qiu, Shuyi; Yu, Shicheng; Zhu, Qicheng; Fan, Bo; Zheng, Chaoran; Li, Guodong; Liang, Shangdong

doi:10.1016/j.brainresbull.2012.10.002

Cited by 33 publications

(17 citation statements)

References 31 publications

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“…After 7 days blood samples were obtained from the tail vein and glycaemia was determined by using a glucometer. Fasting blood glucose >200 mg/dl (11.1 mM) was considered as DM [19,20]. At day 14 the animals were killed by CO 2 inhalation, and L4,5 DRGs were removed.…”

Section: Methodsmentioning

confidence: 99%

Satellite glial cells in dorsal root ganglia are activated in streptozotocin‐treated rodents

Hanani

Blum

Liu

et al. 2014

J Cellular Molecular Medi

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Neuropathic pain is a very common complication in diabetes mellitus (DM), and treatment for it is limited. As DM is becoming a global epidemic it is important to understand and treat this problem. The mechanisms of diabetic neuropathic pain are largely obscure. Recent studies have shown that glial cells are important for a variety of neuropathic pain types, and we investigated what are the changes that satellite glial cells (SGCs) in dorsal root ganglia undergo in a DM type 1 model, induced by streptozotocin (STZ) in mice and rats. We carried out immunohistochemical studies to learn about changes in the activation marker glial fibrillary acidic protein (GFAP) in SGCs. We found that after STZ-treatment the number of neurons surrounded with GFAP-positive SGCs in dorsal root ganglia increased 4-fold in mice and 5-fold in rats. Western blotting for GFAP, which was done only on rats because of the larger size of the ganglia, showed an increase of about 2-fold in STZ-treated rats, supporting the immunohistochemical results. These results indicate for the first time that SGCs are activated in rodent models of DM1. As SGC activation appears to contribute to chronic pain, these results suggest that SGCs may participate in the generation and maintenance of diabetic neuropathic pain, and can serve as a potential therapeutic target.

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Section: Methodsmentioning

confidence: 99%

Satellite glial cells in dorsal root ganglia are activated in streptozotocin‐treated rodents

Hanani

Blum

Liu

et al. 2014

J Cellular Molecular Medi

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“…58 CCL5 has been linked to DM nephropathy 59 and DM cardiovascular autonomic complications. 60 However, during the excisional skin wound repair process, CCL5, through CCR5, promotes bone marrowederived progenitor cells homing to wound sites, hence accelerating wound healing in mice. 61 The suppressed expression of CXCL5 and CCL5 may contribute to the defects in polymorphonuclear neutrophil infiltration and/or progenitor cell generation observed in DM wounded corneas.…”

Section: Il-1ra and Diabetic Cornea Wound Healingmentioning

confidence: 99%

Targeting Imbalance between IL-1β and IL-1 Receptor Antagonist Ameliorates Delayed Epithelium Wound Healing in Diabetic Mouse Corneas

Yan

Gao

Sun

et al. 2016

The American Journal of Pathology

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fanxq@sh163. net.Patients with diabetes mellitus often develop corneal complications and delayed wound healing. How diabetes might alter acute inflammatory responses to tissue injury, leading to delayed wound healing, remains mostly elusive. Using a streptozotocin-induced type I diabetes mellitus mice and corneal epithelium-debridement wound model, we discovered that although wounding induced marked expression of IL-1b and the secreted form of IL-1 receptor antagonist (sIL-1Ra), diabetes suppressed the expressions of sIL-1Ra but not IL-1b in healing epithelia and both in whole cornea. In normoglycemic mice, IL-1b or sIL-1Ra blockade delayed wound healing and influenced each other's expression. In diabetic mice, in addition to delayed reepithelization, diabetes weakened phosphatidylinositol 3-kinaseeAkt signaling, caused cell apoptosis, diminished cell proliferation, suppressed neutrophil and natural killer cell infiltrations, and impaired sensory nerve reinnervation in healing mouse corneas. Local administration of recombinant IL-1Ra partially, but significantly, reversed these pathological changes in the diabetic corneas. CXCL10 was a downstream chemokine of IL-1beIL-1Ra, and exogenous CXCL10 alleviated delayed wound healing in the diabetic, but attenuated it in the normal corneas. In conclusion, the suppressed early innate/inflammatory responses instigated by the imbalance between IL-1b and IL-1Ra is an underlying cause for delayed wound healing in the diabetic corneas. Local application of IL-1Ra accelerates reepithelialization and may be used to treat chronic corneal and potential skin wounds of diabetic patients. (Am J Pathol 2016 http://dx

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“…Control rats (Ctrl) had free access to water and the common diet (which comprised 53% carbohydrate, 23% protein, and 5% fat). The T2DM model was induced by a combination of diet and streptozotocin (STZ) treatment, generating state of islet damage, high sugar levels, and hyperlipidemia [20]. Diabetic rats were fed a homemade high-fat and high-sugar diet (66.5% basal diet, 20% sugar, 10% oil, 2.5% cholesterol, and 1% sodium cholate) for 4 weeks.…”

Section: Methodsmentioning

confidence: 99%

“…Diabetic rats were fed a homemade high-fat and high-sugar diet (66.5% basal diet, 20% sugar, 10% oil, 2.5% cholesterol, and 1% sodium cholate) for 4 weeks. Model rats were injected intraperitoneally with STZ (30 mg/kg) [20], whereas control group rats were injected intraperitoneally with vehicle (citrate buffer, pH 4.4). Experimental rats with fasting blood glucose ≥7.8 mmol/L or random non-fasting blood glucose ≥11.1 mmol/L were considered to be type 2 diabetic rats [20-22].…”

Section: Methodsmentioning

confidence: 99%

“…Model rats were injected intraperitoneally with STZ (30 mg/kg) [20], whereas control group rats were injected intraperitoneally with vehicle (citrate buffer, pH 4.4). Experimental rats with fasting blood glucose ≥7.8 mmol/L or random non-fasting blood glucose ≥11.1 mmol/L were considered to be type 2 diabetic rats [20-22]. Next, diabetic rats were randomly divided into three groups: the diabetic group (DM), the T2DM treated with baicalin group (DM+Bai), and the T2DM treated with normal saline group (DM+NS).…”

Section: Methodsmentioning

confidence: 99%

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Effects of Baicalin on Diabetic Cardiac Autonomic Neuropathy Mediated by the P2Y12 Receptor in Rat Stellate Ganglia

Xuan

Wang²,

Guo

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chronic diabetic hyperglycemia can damage various of organ systems and cause serious complications. Although diabetic cardiac autonomic neuropathy (DCAN) is the primary cause of death in diabetic patients, its pathogenesis remains to be fully elucidated. Baicalin is a flavonoid extracted from Scutellaria baicalensis root and has antibacterial, diuretic, anti-inflammatory, anti- metamorphotic, and antispasmodic effects. Our study explored the effects of baicalin on enhancing sympathoexcitatory response induced by DCAN via the P2Y12 receptor. Methods: A type 2 diabetes mellitus rat model was induced by a combination of diet and streptozotocin. Serum epinephrine was measured by enzyme-linked immunosorbent assay. Blood pressure and heart rate were measured using the indirect tail-cuff method. Heart rate variability was analyzed using the frequency-domain of electrocardiogram recordings. The expression levels of P2Y12, interleukin-1beta (IL-1β), tumor necrosis factor alpha (TNF-α), and connexin 43 (Cx43) were determined by quantitative real-time reverse transcription-polymerase chain reaction and western blotting. The interaction between baicalin and P2Y12 determined using by molecular docking. Results: Baicalin alleviated elevated blood pressure and heart rate, improved heart rate variability, and decreased the elevated expression levels of P2Y12, IL-1β, TNF-α, and Cx43 in the stellate ganglia of diabetic rats. Baicalin also reduced the elevated concentration of serum epinephrine and the phosphorylation of p38 mitogen-activated protein kinase in diabetic rats. Conclusion: Baicalin decreases sympathetic activity by inhibiting the P2Y12 receptor in stellate ganglia satellite glial cells to maintain the balance between sympathetic and parasympathetic nerves and relieves DCAN in the rat.

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Effects of neferine on CCL5 and CCR5 expression in SCG of type 2 diabetic rats

Cited by 33 publications

References 31 publications

Satellite glial cells in dorsal root ganglia are activated in streptozotocin‐treated rodents

Satellite glial cells in dorsal root ganglia are activated in streptozotocin‐treated rodents

Targeting Imbalance between IL-1β and IL-1 Receptor Antagonist Ameliorates Delayed Epithelium Wound Healing in Diabetic Mouse Corneas

Effects of Baicalin on Diabetic Cardiac Autonomic Neuropathy Mediated by the P2Y12 Receptor in Rat Stellate Ganglia

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