Paclitaxel-induced neuropathy induces changes in oral cavity organs of rats

IF 0.5 Q4 BIOLOGY Regulatory Mechanisms in Biosystems Pub Date : 2023-02-07 DOI:10.15421/022315
A. Kotvytska, K. V. Tykhonovych, T. D. Kryvoruchko, K. Neporada, S. Beregovyi
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Abstract

The developmental mechanisms of pathological changes in the oral cavity organs, in particular, periodontal tissues and salivary glands, were elucidated in the model of paclitaxel-induced neuropathy. Experimental studies were performed on 41 white nonlinear rats of both sexes weighing 180–220 g. Toxic neuropathy was modeled by intraperitoneal injection of paclitaxel (Actavis Ltd; series 5GN5122) 2 mg/kg for 4 days (0, 2, 4 and 6). The presence of paclitaxel-induced peripheral neuropathy was confirmed by the Randall-Selitto tensoalgometric test to determine the threshold of pain sensitivity. The total proteolytic activity, total antitryptic activity, and the content of TBA-active products were determined in the homogenate of the rat submandibular and sublingual salivary glands and periodontal soft tissues, content of oxidatively modified proteins, content of average mass molecules and catalase activity; α-amylase activity was also determined in the salivary glands of animals, and the content of free fucose and glycosaminoglycans in periodontal tissues. Paclitaxel-induced neuropathy causes the development of pathological changes in the oral cavity, in particular in periodontal tissues and salivary glands of rats, as evidenced by impaired proteinase-inhibitory potential, intensification of carbonyl oxidative stress, inhibition of protein synthetic function in salivary glands and increased depolymerization of non-collagenous proteins in periodontal soft tissues.
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紫杉醇诱导的神经病变引起大鼠口腔器官的改变
在紫杉醇诱导的神经病变模型中,阐明了口腔器官特别是牙周组织和唾液腺病理变化的发育机制。实验以体重180 ~ 220 g的雌雄非线性大鼠41只为实验对象。通过腹腔注射紫杉醇(Actavis Ltd .;系列5GN5122) 2 mg/kg,连续4天(0,2,4和6)。通过Randall-Selitto张力测量试验确定疼痛敏感阈值,证实紫杉醇诱导的周围神经病变的存在。测定大鼠颌下腺、舌下唾液腺和牙周软组织匀浆中总蛋白水解活性、总抗胰蛋白酶活性、tba活性产物含量、氧化修饰蛋白含量、平均质量分子含量和过氧化氢酶活性;测定动物唾液腺α-淀粉酶活性,牙周组织游离灶和糖胺聚糖含量。紫杉醇诱导的神经病变引起口腔,特别是大鼠牙周组织和唾液腺的病理改变,表现为蛋白酶抑制电位受损,羰基氧化应激加剧,唾液腺蛋白质合成功能抑制,牙周软组织非胶原蛋白解聚增加。
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来源期刊
CiteScore
0.90
自引率
0.00%
发文量
25
审稿时长
10 weeks
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