Ramazan Üstün1, Elif Kaval Oğuz2, Çağrı Delilbaşı3, Ayşe Şeker1, Filiz Taşpınar1, Mehmet Reşit Öncü4, Ahmet Regaip Oğuz5. 1. a Department of Physiology, Faculty of Medicine, Neuroscience Research Unit , Van Yuzuncu Yil University , Van , Turkey. 2. b Department of Science Education, Faculty of Education , Van Yuzuncu Yil University , Van , Turkey. 3. c Department of Oral and Maxillofacial Surgery, School of Dentistry , Istanbul Medipol University , İstanbul , Turkey. 4. d Department of Emergency Medicine, Faculty of Medicine , Van Yuzuncu Yil University , Van , Turkey. 5. e Department of Biology, Science Faculty , Van Yuzuncu Yil University , Van , Turkey.
Abstract
PURPOSE: Ankaferd Blood Stopper® (ABS), a licenced medicinal herbal extract, is commonly used as an effective topical haemostatic agent. This study is designed to investigate whether topical ABS application may cause peripheral nerve degeneration and neuromuscular dysfunction in a mouse sciatic nerve model. METHODS: Twenty mice were randomly divided into two groups; an ABS treated experimental group and a saline-treated control group. Left sciatic nerves were treated with 0.3 ml of ABS in the experimental group and 0.3 ml of sterile saline in the control group for 5 min. Peripheral nerve degeneration and neuromuscular dysfunction were evaluated by behavioural tests, electrophysiological analysis and weight ratio comparison of target muscles. RESULTS: The motor function, assessed by the sciatic function index, was significantly impaired in ABS-treated animals as compared to the animals treated with saline. Motor coordination, evaluated with the rotarod test, was significantly decreased (-42%) in ABS-treated animals compared to the saline-treated animals. The degree of pain, assessed by the reaction latency to thermal stimuli (hot-plate test), was significantly prolonged (313%) in ABS-treated mice when compared to the saline-treated mice. ABS-treated mice showed a significant reduction in motor nerve conduction velocity (MNCV) (-52%) and the compound muscle action potential (CMAP) (-47%); however, it significantly prolonged onset latency (23%). The gastrocnemius muscles weight ratio of the ABS group was considerably lower than that of the control group. CONCLUSIONS: These findings demonstrate that ABS triggers peripheral nerve degeneration and functional impairment and, thus promotes a deterioration of sciatic nerves.
PURPOSE: Ankaferd Blood Stopper® (ABS), a licenced medicinal herbal extract, is commonly used as an effective topical haemostatic agent. This study is designed to investigate whether topical ABS application may cause peripheral nerve degeneration and neuromuscular dysfunction in a mouse sciatic nerve model. METHODS: Twenty mice were randomly divided into two groups; an ABS treated experimental group and a saline-treated control group. Left sciatic nerves were treated with 0.3 ml of ABS in the experimental group and 0.3 ml of sterile saline in the control group for 5 min. Peripheral nerve degeneration and neuromuscular dysfunction were evaluated by behavioural tests, electrophysiological analysis and weight ratio comparison of target muscles. RESULTS: The motor function, assessed by the sciatic function index, was significantly impaired in ABS-treated animals as compared to the animals treated with saline. Motor coordination, evaluated with the rotarod test, was significantly decreased (-42%) in ABS-treated animals compared to the saline-treated animals. The degree of pain, assessed by the reaction latency to thermal stimuli (hot-plate test), was significantly prolonged (313%) in ABS-treated mice when compared to the saline-treated mice. ABS-treated mice showed a significant reduction in motor nerve conduction velocity (MNCV) (-52%) and the compound muscle action potential (CMAP) (-47%); however, it significantly prolonged onset latency (23%). The gastrocnemius muscles weight ratio of the ABS group was considerably lower than that of the control group. CONCLUSIONS: These findings demonstrate that ABS triggers peripheral nerve degeneration and functional impairment and, thus promotes a deterioration of sciatic nerves.