慢性牙周炎对大鼠阴茎海绵体内皮糖萼的影响

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Yuanhang Xia, Yang Zeng, Rui Jiang
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Four weeks after the induction of periodontitis in the rats, the maximum intra‐cavernous pressure/mean arterial pressure (ICPmax/MAP), serum C‐reactive protein (CRP), tumor necrosis factor alpha (TNF‐α), interleukin‐6 (IL‐6), nitric oxide (NO), heparin sulfate (HS), syndecan‐1 (SDC‐1), heparanase (HPSE), eNOS, and phosphor‐eNOS (p‐eNOS) concentration were measured, and the eGlx of the penile corpus cavernosum was observed by transmission electron microscopy (TEM).OutcomesChronic periodontitis can degrade eGlx on the rat penile corpus cavernosum by increasing serum CRP, TNF‐α, and IL‐6 levels, reducing the p‐eNOS/eNOS ratio and the NO concentration in the penile corpus cavernosum, and resulting in the inhibition of the erectile function.ResultsSerum CRP, TNF‐α, and IL‐6 levels and HPSE expression in penile cavernous tissue were significantly greater in the chronic periodontitis group than in the control group and the chronic periodontitis + heparin group (<jats:italic>P</jats:italic> &lt; 0.05). The average thickness of the eGlx muscle in the penile corpus cavernosum in the chronic periodontitis group was significantly lower than those in the control group and chronic periodontitis + heparin group (<jats:italic>P</jats:italic> &lt; 0.05). The HS concentration, SDC‐1 expression, p‐eNOS/eNOS, NO concentration, and ICPmax/MAP in the chronic periodontitis group were significantly lower than those in the control group and chronic periodontitis+ heparin group (<jats:italic>P</jats:italic> &lt; 0.01).Clinical implicationsThe eGlx on penile cavernosum vessels may be a new therapeutic target for the treatment of ED.Strengths and limitationsThis study revealed that chronic periodontitis promotes the decomposition of vascular eGlx in the rat penile corpus cavernosum, however, it is not clear whether chronic periodontitis inhibits the synthesis of eGlx.ConclusionChronic periodontitis can degrade eGlx on the rat penile corpus cavernosum by increasing serum CRP, TNF‐α, and IL‐6 levels, reducing the p‐eNOS/eNOS ratio and the NO concentration in penile cavernous tissue, and resulting in the inhibition of the erectile function. 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引用次数: 0

摘要

背景慢性牙周炎可能诱发勃起功能障碍(ED),但其具体机制尚不清楚。目的研究慢性牙周炎是否会通过影响内皮糖萼(eGlx)而导致勃起功能障碍。方法将24只4周龄雄性Sprague-Dawley大鼠随机分为4组(n = 6):对照组、慢性牙周炎组、慢性牙周炎+肝素组(皮下注射肝素200 U/kg/天,7天)和对照+肝素组。诱导大鼠患牙周炎四周后,大鼠的最大龈腔内压/平均动脉压(ICPmax/MAP)、血清 C 反应蛋白(CRP)、肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)一氧化氮 (NO)、硫酸肝素 (HS)、辛迪加-1 (SDC-1)、肝素酶 (HPSE)、eNOS 和磷-eNOS (p-eNOS) 的浓度,并用透射电子显微镜 (TEM) 观察阴茎海绵体的 eGlx。结果 慢性牙周炎可通过增加血清CRP、TNF-α和IL-6水平,降低p-eNOS/eNOS比值和阴茎海绵体内NO浓度,使大鼠阴茎海绵体的eGlx退化,导致勃起功能受抑制。结果慢性牙周炎组血清 CRP、TNF-α、IL-6 水平和阴茎海绵体组织中 HPSE 表达明显高于对照组和慢性牙周炎 + 肝素组(P < 0.05)。慢性牙周炎组阴茎海绵体 eGlx 肌肉的平均厚度明显低于对照组和慢性牙周炎 + 肝素组(P < 0.05)。慢性牙周炎组的 HS 浓度、SDC-1 表达、p-eNOS/eNOS、NO 浓度和 ICPmax/MAP 均明显低于对照组和慢性牙周炎+肝素组(P < 0.01)。优点和局限性本研究发现,慢性牙周炎会促进大鼠阴茎海绵体血管 eGlx 的分解,但尚不清楚慢性牙周炎是否会抑制 eGlx 的合成。结论 慢性牙周炎可通过增加血清CRP、TNF-α和IL-6水平,降低阴茎海绵体组织中p-eNOS/eNOS比值和NO浓度,从而降解大鼠阴茎海绵体上的eGlx,导致勃起功能受抑制。肝素能抑制慢性牙周炎大鼠体内 eGlx 的分解,改善其勃起功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of chronic periodontitis on the endothelial glycocalyx of rat penile corpus cavernosum
BackgroundChronic periodontitis may induce erectile dysfunction (ED), however, the specific mechanism involved is unclear. The endothelial glycocalyx (eGlx) is a structure that can regulate endothelial nitric oxide synthase (eNOS) phosphorylation on the cavity surface of vessels.AimTo investigate whether chronic periodontitis leads to ED by affecting the eGlx.MethodsTwenty‐four 4‐week‐old male Sprague‒Dawley rats were randomly divided into four groups (n = 6): the control group, chronic periodontitis group, chronic periodontitis + heparin group (subcutaneous heparin 200 U/kg/day, 7 days), and control + heparin group. Four weeks after the induction of periodontitis in the rats, the maximum intra‐cavernous pressure/mean arterial pressure (ICPmax/MAP), serum C‐reactive protein (CRP), tumor necrosis factor alpha (TNF‐α), interleukin‐6 (IL‐6), nitric oxide (NO), heparin sulfate (HS), syndecan‐1 (SDC‐1), heparanase (HPSE), eNOS, and phosphor‐eNOS (p‐eNOS) concentration were measured, and the eGlx of the penile corpus cavernosum was observed by transmission electron microscopy (TEM).OutcomesChronic periodontitis can degrade eGlx on the rat penile corpus cavernosum by increasing serum CRP, TNF‐α, and IL‐6 levels, reducing the p‐eNOS/eNOS ratio and the NO concentration in the penile corpus cavernosum, and resulting in the inhibition of the erectile function.ResultsSerum CRP, TNF‐α, and IL‐6 levels and HPSE expression in penile cavernous tissue were significantly greater in the chronic periodontitis group than in the control group and the chronic periodontitis + heparin group (P < 0.05). The average thickness of the eGlx muscle in the penile corpus cavernosum in the chronic periodontitis group was significantly lower than those in the control group and chronic periodontitis + heparin group (P < 0.05). The HS concentration, SDC‐1 expression, p‐eNOS/eNOS, NO concentration, and ICPmax/MAP in the chronic periodontitis group were significantly lower than those in the control group and chronic periodontitis+ heparin group (P < 0.01).Clinical implicationsThe eGlx on penile cavernosum vessels may be a new therapeutic target for the treatment of ED.Strengths and limitationsThis study revealed that chronic periodontitis promotes the decomposition of vascular eGlx in the rat penile corpus cavernosum, however, it is not clear whether chronic periodontitis inhibits the synthesis of eGlx.ConclusionChronic periodontitis can degrade eGlx on the rat penile corpus cavernosum by increasing serum CRP, TNF‐α, and IL‐6 levels, reducing the p‐eNOS/eNOS ratio and the NO concentration in penile cavernous tissue, and resulting in the inhibition of the erectile function. Heparin inhibited eGlx decomposition and improved erectile function in rats with chronic periodontitis.
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CiteScore
7.20
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4.30%
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