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Effect mechanism research of procyanidin on gingivitis rats by regulating the PI3K/Akt/VEGF signal pathway
- ZHONGGUO YAOFANG Vol. 35, Issue 4, Pages: 436-441(2024)
- 作者机构：
1.张家口学院护理学院，河北 张家口 075000
2.张家口市第一医院口腔科，河北 张家口 075000
- 作者简介：
- 基金信息：
DOI：10.6039/j.issn.1001-0408.2024.04.10
CLC： R965Published：29 February 2024，
Received：22 August 2023，
Revised：29 December 2023，
扫 描 看 全 文
殷晓宁,左宪宏,段丽云等.原花青素通过调节PI3K/Akt/VEGF信号通路对牙龈炎大鼠的作用机制研究 Δ[J].中国药房,2024,35(04):436-441.
YIN Xiaoning,ZUO Xianhong,DUAN Liyun,et al.Effect mechanism research of procyanidin on gingivitis rats by regulating the PI3K/Akt/VEGF signal pathway[J].ZHONGGUO YAOFANG,2024,35(04):436-441.
殷晓宁,左宪宏,段丽云等.原花青素通过调节PI3K/Akt/VEGF信号通路对牙龈炎大鼠的作用机制研究 Δ[J].中国药房,2024,35(04):436-441. DOI： 10.6039/j.issn.1001-0408.2024.04.10.
YIN Xiaoning,ZUO Xianhong,DUAN Liyun,et al.Effect mechanism research of procyanidin on gingivitis rats by regulating the PI3K/Akt/VEGF signal pathway[J].ZHONGGUO YAOFANG,2024,35(04):436-441. DOI： 10.6039/j.issn.1001-0408.2024.04.10.
摘要
目的
2
探讨原花青素通过调节磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/血管内皮生长因子（VEGF）信号通路对牙龈炎大鼠的潜在作用机制。
方法
2
通过丝线缝扎大鼠上颌双侧第1磨牙牙颈部+涂抹麦芽糖+喂食20%蔗糖溶液及软食的方法构建牙龈炎大鼠模型，将造模成功的48只大鼠随机分为模型组、原花青素组（160 mg/kg）、740Y-P组（PI3K/Akt信号通路激活剂，0.02 mg/kg）、原花青素+740Y-P组（原花青素160 mg/kg+740Y-P 0.02 mg/kg），每组12只；另取12只大鼠作为对照组。各药物组大鼠灌胃或/和腹腔注射相应药液，每天1次，连续7 d。末次给药结束24 h后，测定大鼠牙龈指数，检测其龈沟液中白细胞介素18（IL-18）、诱导型一氧化氮合酶（iNOS）、碱性磷酸酶（ALP）水平以及牙龈组织中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、活性氧（ROS）水平，观察大鼠牙龈组织的病理形态并检测其牙龈组织中PI3K/Akt/VEGF信号通路相关蛋白的表达情况。
结果
2
与对照组比较，模型组大鼠牙龈组织存在局部组织扩张充血、新生毛细血管出现、胶原纤维变性丢失且排列紊乱、大量炎症细胞浸润龈沟壁等病理改变；其牙龈指数，龈沟液中IL-18、iNOS、ALP水平，牙龈组织中ROS水平，PI3K、Akt蛋白的磷酸化水平以及VEGF蛋白的表达水平均显著升高，牙龈组织中SOD、CAT水平显著降低（
P
＜0.05）。与模型组比较，原花青素组大鼠牙龈组织病理损伤减轻，上述各定量指标均显著改善（
P
＜0.05），且740Y-P能逆转原花青素对各指标的改善作用（
P
＜0.05）。
结论
2
原花青素可能通过抑制PI3K/Akt/VEGF信号通路来缓解牙龈炎大鼠的牙龈组织损伤，改善牙龈炎症和氧化应激。
Abstract
OBJECTIVE
2
To investigate the potential mechanism of procyanidin on rats with gingivitis by regulating phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt）/vascular endothelial growth factor （VEGF） signaling pathway.
METHODS
2
The rat model of gingivitis was constructed by sewing the neck of the first maxillary molar with silk thread+applying maltose on the gum+feeding with 20% sucrose solution and soft food. Forth-eight model rats were randomly divided into model group， procyanidin group （160 mg/kg）， 740Y-P group （PI3K/Akt signaling pathway activator， 0.02 mg/kg）， and procyanidin+740Y-P group （procyanidin 160 mg/kg+740Y-P 0.02 mg/kg）， with 12 rats in each group； another 12 rats were selected as control group； each medication group was treated with corresponding drugs intragastrically or/and intraperitoneally， once a day， for 7 consecutive days. Twenty-four hours after the last administration， the gingival index of rats was measured； the levels of interleukin-18 （IL-18）， inducible nitric oxide synthase （iNOS） and alkaline phosphatase （ALP） in gingival crevicular fluid， as well as the levels of superoxide dismutase （SOD）， catalase （CAT） and reactive oxygen species （ROS） in gingival tissues of rats were detected； the pathological changes in gingival tissues were observed； the expression levels of PI3K/Akt/VEGF signaling pathway-related proteins in gingival tissues of rats were detected.
RESULTS
2
Compared with control group， the gingival tissues of rats in the model group had severe pathological damage， which was manifested as local tissue expansion and congestion， new capillaries， degeneration and loss of collagen fibers and disorder of arrangement， and a large number of inflammatory cell infiltration in the gingival sulcus wall. The gingival index， the levels of IL-18， iNOS， ALP in gingival crevicular fluid， the level of ROS in gingival tissues， the phosphorylations of PI3K and Akt， as well as the protein expression of VEGF in gingival tissues were significantly increased； the levels of SOD and CAT in gingival tissues of rats in model group were significantly decreased （
P
＜0.05）. Compared with model group， the pathological damage to the gingival tissues of rats in procyanidin group was reduced， and all quantitative indicators were significantly improved （
P
＜0.05）； 740Y-P could reverse the improvement effect of procyanidin on various indicators （
P
＜0.05）.
CONCLUSIONS
2
Procyanidin may alleviate gingival tissue damage， and improve gingival inflammation and oxidative stress in rats with gingivitis by inhibiting PI3K/Akt/VEGF signaling pathway.
关键词
原花青素牙龈炎牙龈组织磷脂酰肌醇3激酶/蛋白激酶B/血管内皮生长因子信号通路
Keywords
gingivitisgingival tissuephosphoinositide 3-kinase/protein kinase B/vascular endothelial growth factor signaling pathway
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