Pérdida y Desprendimiento de Pericitos en la Neuropatía Experimental Inducida por Cisplatino Depicha Jindatip; Worapat Nopparat; Phetnarin Kobutree; Atitaya Roumwong & Sithiporn Agthong JINDATIP, D.; NOPPARAT, W.; KOBUTREE, P.; ROUMWONG, A. & AGTHONG, S. Pericyte loss and detachment in experimental cisplatin-induced neuropathy. Int. J. Morphol., 37(2):509-514, 2019. SUMMARY:Cisplatin is an antineoplastic agent with neuropathy as one of its major side effect. However, effective treatment is lacking. Increasing evidence suggests that cisplatin might damage nerve capillaries leading to impaired functions of blood-nerve barrier (BNB) and neuropathy. This study was aimed to examine the effects of cisplatin on pericytes. Rats were either treated with intraperitoneal injection of cisplatin 2 mg/kg twice a week for five continuous weeks. Cisplatin-treated rats showed reduced body weight, thermal hypoalgesia and slow sciatic motor nerve conduction velocity, indicating neuropathy. The density of pericytes in the distal sciatic nerves determined by immunohistochemistry to desmin was significantly reduced in the cisplatin compared with that of the control groups. Electron microscopic analysis demonstrated the detachment of pericytes from endothelial cells including the disruption of shared basement membrane in the sciatic nerves from cisplatin-treated rats. These data indicate the pericyte loss and detachment caused by cisplatin. Future studies of the BNB components and functions after cisplatin treatment are needed and will be essential for the development of effective treatments against cisplatin-induced neuropathy.

A standardized extract of Centella asiatica (ECa 233) prevents temporomandibular joint osteoarthritis by modulating the expression of local inflammatory mediators in mice Objectives: To investigate the effect of a standardized extract of Centella asiatica (ECa 233), which has anti-inflammatory properties, on the local expression of the transient receptor potential vanilloid 1 (TRPV1), the acidsensing ion channel subunit 3 (ASIC3), and the calcitonin gene-related peptide (CGRP) in the temporomandibular joint (TMJ) structure 21 days after injecting the TMJ with complete Freund's adjuvant (CFA). Methodology: A mouse model was induced by analyzing the CFA-injected TMJ on days 7, 14, and 21. We assessed TMJ histology by the osteoarthritis cartilage grade score. Then, we observed the effect of different ECa 233 concentrations (30, 100, and 300 mg/kg) and of 140 mg/kg ibuprofen doses on TRPV1, ASIC3, and CGRP local expression on day 21. Results: Osteoarthritis cartilage scores were 1.17±0.37 and 3.83±0.68 on days 14 and 21, respectively, in the CFA group (n=5). On day 21, TRPV1, ASIC3, and CGRP expression significantly increased in the CFA group. In the ibuprofen-treated group, TRPV1 expression significantly decreased, but ASIC3 and CGRP showed no significant difference. All ECa 233 doses reduced TRPV1 expression, but the 100 mg/kg ECa 233 dose significantly decreased ASIC3 expression. Conclusions: TRPV1, ASIC3, and CGRP expression increased in mice with TMJ-OA on day 21. All ECa 233 and ibuprofen doses inhibited pathogenesis by modulating the local expression of TRPV1 and ASIC3. Therefore, ECa 233 was more effective than ibuprofen.

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Prolonged inflammation causing tissue injury can induce chronic pain hypersensitivity (allodynia and hyperalgesia). Osteoarthritis of the temporomandibular joint (TMJ-OA) is a common cause of chronic allodynia encountered in dental practice, but many currently available treatments induce intolerable side effects. In this study, we investigated the potential efficacy of a standardized Centella asiatica extract (ECa 233) on allodynia in a TMJ-OA mouse model established by an injection of complete Freund's adjuvant (CFA) into the TMJ. After CFA injection, animals daily received oral administration of vehicle, 0.14 g/kg ibuprofen (positive control), 30 mg/kg ECa 233, or 100 mg/kg ECa 233. Behavioral pain responses were examined by air-puff tests before and after CFA injection on days 3, 7, 14, 21, and 28. On day 28, TMJ-OA pathology was assessed by changes in articular cartilage thickness and graded according to the Osteoarthritis Cartilage Histopathology Assessment (OCHA) system. In the CFA + vehicle group, pain response scores increased gradually, reaching statistical significance compared to untreated Sham controls on days 14, 21, and 28. On day 28, OCHA grade score was 3.5 ± 0.35, and articular cartilage thickness was reduced compared to the Sham group. Both ECa 233 doses significantly attenuated pain response scores and also slowed degeneration of the TMJ with efficacy comparable to ibuprofen. We conclude that ECa 233 can protect against mechanical allodynia and cartilage degeneration in a mouse model of TMJ-OA.

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