RESUMO: "Produtos naturais inibidores da enzima acetilcolinesterase". A Doença de Alzheimer (DA) é uma patologia neurodegenerativa, progressiva, que afeta principalmente a população idosa, responsável por 50-60% dos casos de demência em pessoas com mais de 65 anos de idade. Os principais sintomas associado a DA envolve defi ciência orgânica cognitiva, principalmente perda de memória. Outras características associadas com os estágios avançados de DA inclui défi cit na linguagem, depressão, problemas de comportamento, inclusive agitação, alterações de humor e psicose.Um dos mais promissores caminhos para tratar esta doença é aumentar o nível de acetilcolina no cérebro usando inibidores da acetilcolinesterase (AChE). Este trabalho teve como objetivo revisar a literatura das plantas e substâncias encontradas nas plantas, inibidores da enzima acetilcolinesterase. Foram levantadas 309 plantas e 260 substâncias isoladas de plantas que foram classifi cados em grupos químicos adequados, os modelo testados, e suas atividades. Foram consultados 175 referências.Unitermos: Inibidores da Acetilcolinesterase, AchE, doença de Alzheimer, distúrbios neurodegenetivos, plantas medicinais, produtos naturais, revisão.ABSTRACT: Alzheimer's disease (AD) is a progressive, neurodegenerative pathology that primarily affects the elderly population, and is estimated to account for 50-60% of dementia cases in persons over 65 years of age. The main symptoms associated with AD involve cognitive dysfunction, primarily memory loss. Other features associated with the later stages of AD include language defi cits, depression, behavioural problems including agitation, mood disturbances and psychosis. One of the most promising approaches for treating this disease is to enhance the acetylcholine level in the brain using acetylcholinesterase (AChE) inhibitors. The present work reviews the literature on plants and plant-derived compounds inhibitors of enzyme acetylcholinesterase. The review refers to 309 plant extracts and 260 compounds isolated from plants, which are classifi ed in appropriate chemical groups and model tested, and cites their activity. For this purpose 175 references were consulted.
RESUMO:O medicamento fi toterápico brasileiro -BPF é composto de corantes das plantas Eucalyptus globulus Labill, Peltodon radicans Pohl e Schinus terebinthifolius Raddi em alcool a 13,3° GL. Este medicamento é popularmente usado no estado da Paraíba, Brasil desde 1889 como anti-séptico e antiinfl amatório. O objetivo deste estudo foi avaliar a propriedade antiinfl amatória deste medicamento fi toterápico. Para tal, foram utilizadas as técnicas de edema de orelha em camundongos induzido por 12-O-tetradecanoilforbol 13-acetato (TPA) ou capsaicina e o edema de pata de rato induzido por carragenina. O BPF na dose de 26 mL/kg inibiu tanto edema de orelha induzido por TPA como por capsaicina a 49% (p < 0.05) e 24% (p < 0.01) respectivamente. Estudos preliminares utilizando a técnica de edema de pata induzido por carragenina demonstraram que a administração oral também inibiu o edema de pata em aproximadamente 29%. Os resultados demonstraram que o medicamento fi toterápico brasileiro (BPF) apresentou propriedades antiinfl amatórias e a melhor dose foi aquela que é usada pela população. Unitermos:Medicamento fi toterápico brasileiro, atividade antiinfl amatória, capsaicina, 12-Otetradecanoilforbol 13-acetato. ABSTRACT: The Brazilian polyherbal formulation (BPF) is composed by dyes of Eucalyptus globulus Labill, Peltodon radicans Pohl and Schinus terebinthifoliusRaddi in alcohol at 13.3° GL. The formulation is popularly used in Paraíba state, Brazil since 1889 and it is used as an antiseptic and anti-infl ammatory medicine. The aim of this study was to evaluate the anti-infl ammatory property of the polyherbal formulation. For this purpose it was used the12-O-tetradecanoylphorbol 13-acetate (TPA) and capsaicin-induced mouse ear edema and the carrageenan-induced rat paw edema. The BPF at dose of 26 mL/Kg inhibited both 12-O-tetradecanoylphorbol 13-acetate (TPA) and capsaicin-induced ear edema by 49% (p < 0.05) and 24% (p < 0.01) respectively. Preliminary results on carrageenan-induced rat paw edema demonstrated that oral administration also inhibited the paw edema by approximately 29%. The results demonstrate that the Brazilian polyherbal formulation has anti-infl ammatory activity and the better dose was the one used by the population.
Asthma is a chronic respiratory disease characterized by airway inflammation and airway hyperresponsiveness (AHR). One strategy to treat allergic diseases is the development of new drugs. Flavonoids are compounds derived from plants and are known to have antiallergic, anti-inflammatory, and antioxidant properties. To investigate whether the flavonoid kaempferol glycoside 3-O-[beta-d-glycopiranosil-(1-->6)-alpha-l-ramnopiranosil]-7-O-alpha-l-ramnopiranosil-kaempferol (GRRK) would be capable of modulating allergic airway disease (AAD) either as a preventive (GRRK P) or curative (GRRK C) treatment in an experimental model of asthma. At weekly intervals, BALB/c mice were subcutaneously (sc) sensitized twice with ovalbumin (OVA)/alum and challenged twice with OVA administered intranasally. To evaluate any preventive effect, GRRK was administered 1h (hour) before each OVA-sensitization and challenge, while to analyze the curative effect, mice were first sensitized with OVA, followed by GRRK given at day 18 through 21. The onset of AAD was evaluated 24h after the last OVA challenge. Both treatments resulted in a dose-dependent reduction in total leukocyte and eosinophil counts in the bronchoalveolar lavage fluid (BAL). GRRK also decreased CD4(+), B220(+), MHC class II and CD40 molecule expressions in BAL cells. Histology and lung mechanic showed that GRRK suppressed mucus production and ameliorated the AHR induced by OVA challenge. Furthermore, GRRK impaired Th2 cytokine production (IL-5 and IL-13) and did not induce a Th1 pattern of inflammation. These findings demonstrate that GRRK treatment before or after established allergic lung disease down-regulates key asthmatic features. Therefore, GRRK has a potential clinical use for the treatment of allergic asthma.
The antitumor effects of thiophene and acridine compounds have been described; however, the clinical usefulness of these compounds is limited due to the risk of high toxicity and drug resistance. The strategy of molecular hybridization presents the opportunity to develop new drugs which may display better target affinity and less serious side effects. Herein, 2-((6-Chloro-2-methoxy-acridin-9-yl)amino)-5,6,7,8-tetrahydro-4H-cyclohepta[b]-thiophene-3-carbonitrile (ACS03), a hybrid thiophene–acridine compound with antileishmanial activity, was tested for toxicity and antitumor activity. The toxicity was evaluated in vitro (on HaCat and peripheral blood mononuclear cells) and in vivo (zebrafish embryos and acute toxicity in mice). Antitumor activity was also assessed in vitro in HCT-116 (human colon carcinoma cell line), K562 (chronic myeloid leukemic cell line), HL-60 (human promyelocytic leukemia cell line), HeLa (human cervical cancer cell line), and MCF-7 (breast cancer cell line) and in vivo (Ehrlich ascites carcinoma model). ACS03 exhibited selectivity toward HCT-116 cells (Half maximal inhibitory concentration, IC50 = 23.11 ± 1.03 µM). In zebrafish embryos, ACS03 induced an increase in lactate dehydrogenase, glutathione S-transferase, and acetylcholinesterase activities. The LD50 (lethal dose 50%) value in mice was estimated to be higher than 5000 mg/kg (intraperitoneally). In vivo, ACS03 (12.5 mg/kg) induced a significant reduction in tumor volume and cell viability. In vivo antitumor activity was associated with the nitric oxide cytotoxic effect. In conclusion, significant antitumor activity and weak toxicity were recorded for this hybrid compound, characterizing it as a potential anticancer compound.
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