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1.
Cutan Ocul Toxicol ; 41(1): 18-24, 2022 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-35100933

RESUMO

PURPOSE: In the treatment of cutaneous leishmaniasis (CL), developing drug resistance, existing toxic effects of drugs and failure respond to treatment cause the need to try different treatment methods. We investigated the effect of gold-conjugated macrophage-specific antibody on amastigotes under infra-red light for the treatment of CL. METHODS: Female BALB/c (4-8 weeks old, 20 ± 5 g weight) mice were used in the study. The L. major strain was inoculated on the soles of mice in amastigote form and subpassed. Nanogold (Au), Au + macrophage-specific antibody (MSA) modification and near infra-red (NIR) (5 seconds) were applied to mice groups that developed cutaneous leishmaniasis on their soles. On the 5th and 10th days of the treatment, the lesions were examined clinically and pathologically. RESULTS: When the erythema values were examined, the highest decrease was calculated in the Au + MSA + NIR group in the measurements made on the 10th day (p < 0.014). The best improvement in 10th day measurements is in the NIR and Au + MSA + NIR groups when area values were examined (p = 0.011, p = 0.001). There was a statistically significant difference between the groups in terms of parasite load (PL) (p < 0.005) in pathological evaluation. According to PL grouping, the best result is NIR (p = 0.002). When both main titles (clinical and pathological) are examined, the Au + MSA + NIR group is thought to have an optimal therapeutical feature. CONCLUSIONS: Au + MSA + NIR combination could be a new treatment approach for CL treatment.


Assuntos
Leishmania major , Leishmaniose Cutânea , Animais , Feminino , Leishmaniose Cutânea/tratamento farmacológico , Macrófagos , Camundongos , Camundongos Endogâmicos BALB C , Carga Parasitária
2.
Cutan Ocul Toxicol ; 37(1): 24-28, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-28468507

RESUMO

BACKGROUND: Numerous growth factors, cytokine, mitogen and chemotactic factors are involved in wound healing. Even though inflammation is important for the stimulation of proliferative phase, excessive inflammation also causes impairment in wound healing. Strontium salts suppress keratinocyte-induced TNF-alpha and interleukin-1 and interleukin-6 in in vitro cultures. This study was conducted to determine the effects of administration of topical strontium chloride hexahydrate on wound healing through TNF-alpha and TGF-beta in surgical wound healing model of in-vivo rat skin. MATERIAL AND METHODS: Twenty-four rats were used in the study. After approximately 2 cm cutaneous-subcutaneous incision was horizontally carried out on the mid-neckline of the rats, the incision was again closed using 2.0 vicryl. The rats were assigned into three groups including eight rats in each group. Placebo emollient ointment and also the ointments, which were containing 5% and 10% strontium chloride hexahydrate and were prepared at the same base with placebo ointment, were administered to the groups by a blind executor twice a day for a week. At the end of seventh day, the rats were sacrificed and cutaneous and subcutaneous tissue of their wound site was resected for histopathological examination. Scoring of histopathological wound healing and scoring of tissue TNF-alpha and TGF-beta level with immunohistochemical staining were performed. RESULTS: The groups, to which both 5% and 10% strontium chloride hexahydrate was administered, had lower immunohistochemical TNF-alpha levels and histopathological wound scores compared to controls, which was statistically significant (p < 0.05). CONCLUSION: Strontium chloride hexahydrate can lead to impairment in wound healing by suppressing inflammation through TNF-alpha.


Assuntos
Estrôncio/farmacologia , Fator de Necrose Tumoral alfa/imunologia , Cicatrização/efeitos dos fármacos , Administração Cutânea , Animais , Procedimentos Cirúrgicos Dermatológicos , Feminino , Inflamação/imunologia , Ratos Wistar , Pele/efeitos dos fármacos , Pele/imunologia , Pele/patologia , Fator de Crescimento Transformador beta/imunologia
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