激动剂/拮抗剂作用下大鼠牙周组织α7nAChR表达的研究
摘要
吸烟是慢性牙周炎的主要危险因素。吸烟相关性牙周炎的典型特征是牙周附着丧失,牙周袋形成,牙槽骨缺失,最终导致牙齿缺失。尼古丁作为烟草中的主要生物碱,对牙周组织可造成多种损害,但确切的作用机制至今仍未明了。研究发现,α7烟碱型乙酰胆碱受体(α7 nicotine acetylcholine receptor,α7 nAChR)可能与烟草毒性相关。本研究拟在前期研究的基础上,通过牙周炎动物模型,MicroCT,免疫组化等技术手段,研究α7 nAChR在大鼠牙周组织的分布及其在受体激动剂尼古丁,拮抗剂美加明、α-银环蛇毒素作用下表达的改变,及相应牙周组织炎症的变化情况,以期探讨α7nAChR在尼古丁与牙周炎发生发展中的作用,为寻找新的牙周炎防治途径提供理论和实验依据。
1尼古丁/美加明作用下大鼠牙周组织α7nAChR的表达
雄性SD大鼠16只,200g±10g。应用丝线结扎上颌右侧第二磨牙,建立实验性牙周炎模型,将其随机分为对照组(C),生理盐水组(S),尼古丁组(NT),尼古丁+美加明组(MEC),每组4只。分别于首次给药后第14、28天处死每组各一半大鼠。通过牙周临床指标检测及HE染色观察牙周组织炎症程度,利用免疫组化及半定量分析,观察比较上颌第二磨牙牙周组织中α7 nAChR的表达。结果显示,实验性牙周炎大鼠牙周膜成纤维细胞、成骨细胞等均可见α7nAChR阳性染色;与对照组相比,尼古丁组牙周膜α7 nAChR染色增强(P<0.05),同时龈沟出血指数和牙周探诊深度值增高(P<0.05);而受体拮抗剂美加明可抑制尼古丁的作用(P<0.05)。初步证实,α7 nAChR可能作为尼古丁的靶受体,在吸烟相关性牙周炎的发生发展中发挥了重要作用。
2尼古丁/α-BTX作用下大鼠牙周组织α7nAChR的表达
雄性SD大鼠24只,体重180±20g。随机分为对照组,生理盐水组(S),尼古丁组(NT),尼古丁+α-BTX (BTX)(n=6)。其中对照组右侧为单纯丝线结扎对照(L),左侧为空白对照(C)。大鼠麻醉状态下,采用3-0丝线结扎对照组右侧,及其他组双侧上颌第二磨牙颈部。次日起,NT组腹腔注射尼古丁1.7mg/kg/d。BTX组在尼古丁给药前30分钟,腹腔注射α-BTX 10μg /kg/d,S组注射等量生理盐水。分别于首次给药后第14、28天处死每组各一半大鼠。取双侧上颌磨牙段,行MicroCT扫描分析,并常规制作石蜡切片。
大体检查及HE结果显示,尼古丁可以加重丝线结扎引起的牙周炎症状,提前给予α-BTX,可在一定程度上遏制尼古丁的作用。Microview三维分析结果显示,28天时,L,S组与C组相比,有明显的牙槽骨丧失(P<0.05),且L,S组间无明显差异(P>0.05);NT组与L,S组相比,牙槽骨丧失更为显著(P<0.05);BTX组与NT组相比,牙槽骨丧失较轻(P<0.05);但BTX组与L组相比,有差异但无统计学意义(P>0.05)。免疫组化结果表明,给予尼古丁后,大鼠牙周膜组织中α7 nAChR的表达增强;而预先给予受体拮抗剂α-BTX,则尼古丁对α7 nAChR的上调作用受到明显抑制。
这进一步证实,α7 nAChR可能作为尼古丁的靶受体,在吸烟相关性牙周炎的发生发展中发挥了重要作用。
It’s well known that smoking is the major risk factor for chronic periodontal disease. Tobacco-related periodontal disease is characterized as the destruction of periodontal supporting tissues, bone loss, attachment loss, and pocket formation, which finally lead to loss of teeth. Nicotine, as the main alkaloid in tobacco, can cause a variety of damage on the periodontal tissue, but the exact mechanism is not yet fully understood. In recent studies,α7 nicotinic acetylcholine receptor (α7 nAChR) has been found connected with the tobacco-related toxicity.
The objective of this study is to investigate the expression and function ofα7 nicotinic acetylcholine receptor (α7 nAChR) in the periodontal membrane of rat with experimental periodontitis. The main contents and results are described as follows.
1. The effects of nicotine/mecamylamine on the expression ofα7nAChR in rat periodontal tissue and the development of experimental periodontitis.
Experimental periodontitis was induced by ligaturing the cervix of the right second maxillary molar with 3-0 thread of 16 SD male adult rats. On the following day, the animals were assigned into 4 groups: control(C) group, saline(S) group, nicotine(NT)group and nicotine +mecamylamine(MEC) group(n=4). NT group intraperitonealy injected with nicotine (1.7mg/kg/d), and MEC group were intraperitonealy injected with mecamylamine (1mg/kg/d), followed 30 min later by injection of nicotine (1.7mg/kg/d). 14 and 28 days after ligation, half rats were sacrificed respectively in each group. Clinical and histological examinations were used to evaluate the degree of the periodontitis.α7 nAChR in the periodontal membrane of rats was examined using immuno-histochemical techniques.
α7 nAChR was mainly found in the fibroblasts and osteoblast. Nicotine significantly increased the values of sulcular bleeding index (SBI) and probe depth (PD) (P<0.05), and enhanced the expression ofα7nAChR in periodontal membrane (P<0.05). But the MEC can block the effect of the nicotine (P<0.05).
α7nAChR may play an important role in the development of tobacco-related periodontitis.
2. The effects of nicotine/α-BTX on the expression ofα7nAChR in rat periodontal tissue and the development of experimental periodontitis.
24 male SD rats were randomly assigned into 4 groups: control(C) group, saline(S) group, nicotine (NT) group and nicotine +α-BTX(BTX) group(n=6). On the following day, the cervixes of the both sides second maxillary molar were ligatured with 3-0 silk thread. The left sides of control group were not ligatured as the blank control (C), and right sides were ligatured as the positive control (L). NT group intraperitonealy injected with nicotine (1.7mg/kg/d), and BTX group were intraperitonealy injected withα-BTX (10mg/kg/d), followed 30 min later by injection of nicotine (1.7mg/kg/d). 14 and 28 days after ligation, half rats were sacrificed respectively in each group. Clinical, histological, and MicroCT examinations were used to evaluate the degree of the periodontitis.α7 nAChR in the periodontal membrane of rats was examined using immuno-histochemical techniques.
Clinical examination and HE showed that nicotine can increase the thread ligation-induced periodontitis symptoms, and if given earlyα-BTX, the effects of nicotine would be obviously suppressed. MicroCT analysis showed that compared with the C group, the alveolar bone significantly decreased (P <0.05). L and S group showed no significant difference (P>0.05). NT group had significantly more alveolar bone loss than that of L and S group (P <0.05). BTX group compared with the NT group, showed less alveolar bone loss (P <0.05). BTX group and L, S group showed no significant difference (P> 0.05). Further BMD, BVF, TB.Sp, TB.Th also displayed similar results. Immunohistochemistry results revealed that nicotine enhanced the expression ofα7 nAChR in periodontal ligament tissue of rats.α-BTX pretreatment of nicotine-treated rats abrogated the increasedα7nAChR expression.
The results indicate that nicotine enhances susceptibility to periodontitis viaα7 nAChR, which may act via suppressing protective immune responses through the cholinergic anti-inflammatory pathway.
1尼古丁/美加明作用下大鼠牙周组织α7nAChR的表达
雄性SD大鼠16只,200g±10g。应用丝线结扎上颌右侧第二磨牙,建立实验性牙周炎模型,将其随机分为对照组(C),生理盐水组(S),尼古丁组(NT),尼古丁+美加明组(MEC),每组4只。分别于首次给药后第14、28天处死每组各一半大鼠。通过牙周临床指标检测及HE染色观察牙周组织炎症程度,利用免疫组化及半定量分析,观察比较上颌第二磨牙牙周组织中α7 nAChR的表达。结果显示,实验性牙周炎大鼠牙周膜成纤维细胞、成骨细胞等均可见α7nAChR阳性染色;与对照组相比,尼古丁组牙周膜α7 nAChR染色增强(P<0.05),同时龈沟出血指数和牙周探诊深度值增高(P<0.05);而受体拮抗剂美加明可抑制尼古丁的作用(P<0.05)。初步证实,α7 nAChR可能作为尼古丁的靶受体,在吸烟相关性牙周炎的发生发展中发挥了重要作用。
2尼古丁/α-BTX作用下大鼠牙周组织α7nAChR的表达
雄性SD大鼠24只,体重180±20g。随机分为对照组,生理盐水组(S),尼古丁组(NT),尼古丁+α-BTX (BTX)(n=6)。其中对照组右侧为单纯丝线结扎对照(L),左侧为空白对照(C)。大鼠麻醉状态下,采用3-0丝线结扎对照组右侧,及其他组双侧上颌第二磨牙颈部。次日起,NT组腹腔注射尼古丁1.7mg/kg/d。BTX组在尼古丁给药前30分钟,腹腔注射α-BTX 10μg /kg/d,S组注射等量生理盐水。分别于首次给药后第14、28天处死每组各一半大鼠。取双侧上颌磨牙段,行MicroCT扫描分析,并常规制作石蜡切片。
大体检查及HE结果显示,尼古丁可以加重丝线结扎引起的牙周炎症状,提前给予α-BTX,可在一定程度上遏制尼古丁的作用。Microview三维分析结果显示,28天时,L,S组与C组相比,有明显的牙槽骨丧失(P<0.05),且L,S组间无明显差异(P>0.05);NT组与L,S组相比,牙槽骨丧失更为显著(P<0.05);BTX组与NT组相比,牙槽骨丧失较轻(P<0.05);但BTX组与L组相比,有差异但无统计学意义(P>0.05)。免疫组化结果表明,给予尼古丁后,大鼠牙周膜组织中α7 nAChR的表达增强;而预先给予受体拮抗剂α-BTX,则尼古丁对α7 nAChR的上调作用受到明显抑制。
这进一步证实,α7 nAChR可能作为尼古丁的靶受体,在吸烟相关性牙周炎的发生发展中发挥了重要作用。
It’s well known that smoking is the major risk factor for chronic periodontal disease. Tobacco-related periodontal disease is characterized as the destruction of periodontal supporting tissues, bone loss, attachment loss, and pocket formation, which finally lead to loss of teeth. Nicotine, as the main alkaloid in tobacco, can cause a variety of damage on the periodontal tissue, but the exact mechanism is not yet fully understood. In recent studies,α7 nicotinic acetylcholine receptor (α7 nAChR) has been found connected with the tobacco-related toxicity.
The objective of this study is to investigate the expression and function ofα7 nicotinic acetylcholine receptor (α7 nAChR) in the periodontal membrane of rat with experimental periodontitis. The main contents and results are described as follows.
1. The effects of nicotine/mecamylamine on the expression ofα7nAChR in rat periodontal tissue and the development of experimental periodontitis.
Experimental periodontitis was induced by ligaturing the cervix of the right second maxillary molar with 3-0 thread of 16 SD male adult rats. On the following day, the animals were assigned into 4 groups: control(C) group, saline(S) group, nicotine(NT)group and nicotine +mecamylamine(MEC) group(n=4). NT group intraperitonealy injected with nicotine (1.7mg/kg/d), and MEC group were intraperitonealy injected with mecamylamine (1mg/kg/d), followed 30 min later by injection of nicotine (1.7mg/kg/d). 14 and 28 days after ligation, half rats were sacrificed respectively in each group. Clinical and histological examinations were used to evaluate the degree of the periodontitis.α7 nAChR in the periodontal membrane of rats was examined using immuno-histochemical techniques.
α7 nAChR was mainly found in the fibroblasts and osteoblast. Nicotine significantly increased the values of sulcular bleeding index (SBI) and probe depth (PD) (P<0.05), and enhanced the expression ofα7nAChR in periodontal membrane (P<0.05). But the MEC can block the effect of the nicotine (P<0.05).
α7nAChR may play an important role in the development of tobacco-related periodontitis.
2. The effects of nicotine/α-BTX on the expression ofα7nAChR in rat periodontal tissue and the development of experimental periodontitis.
24 male SD rats were randomly assigned into 4 groups: control(C) group, saline(S) group, nicotine (NT) group and nicotine +α-BTX(BTX) group(n=6). On the following day, the cervixes of the both sides second maxillary molar were ligatured with 3-0 silk thread. The left sides of control group were not ligatured as the blank control (C), and right sides were ligatured as the positive control (L). NT group intraperitonealy injected with nicotine (1.7mg/kg/d), and BTX group were intraperitonealy injected withα-BTX (10mg/kg/d), followed 30 min later by injection of nicotine (1.7mg/kg/d). 14 and 28 days after ligation, half rats were sacrificed respectively in each group. Clinical, histological, and MicroCT examinations were used to evaluate the degree of the periodontitis.α7 nAChR in the periodontal membrane of rats was examined using immuno-histochemical techniques.
Clinical examination and HE showed that nicotine can increase the thread ligation-induced periodontitis symptoms, and if given earlyα-BTX, the effects of nicotine would be obviously suppressed. MicroCT analysis showed that compared with the C group, the alveolar bone significantly decreased (P <0.05). L and S group showed no significant difference (P>0.05). NT group had significantly more alveolar bone loss than that of L and S group (P <0.05). BTX group compared with the NT group, showed less alveolar bone loss (P <0.05). BTX group and L, S group showed no significant difference (P> 0.05). Further BMD, BVF, TB.Sp, TB.Th also displayed similar results. Immunohistochemistry results revealed that nicotine enhanced the expression ofα7 nAChR in periodontal ligament tissue of rats.α-BTX pretreatment of nicotine-treated rats abrogated the increasedα7nAChR expression.
The results indicate that nicotine enhances susceptibility to periodontitis viaα7 nAChR, which may act via suppressing protective immune responses through the cholinergic anti-inflammatory pathway.
引文
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