α-Tocopherol and ascorbic acid supplementation reduced acute lung inflammatory response by cigarette smoke in mouse

Bezerra, Frank Silva; Valença, Samuel Santos; Lanzetti, Manuella; Pimenta, Wagner Alves; Castro, Priscila da Silva; Koatz, Vera Lúcia Gonçalves; Pôrto, Luís Cristóvão

doi:10.1016/j.nut.2006.08.016

Cited by 55 publications

(33 citation statements)

References 44 publications

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“…The visualization of the alveolar macrophages in some immunostained slides was confirmed by Giemsa staining. (17,18) Numerical data were calculated as mean ± standard error. For continuous data, the differences among the groups were determined using analysis also play a role in regulating inflammation through the generation of chemokines and cytokines and by creating openings in the tissue barriers for the passage of inflammatory cells.…”

Section: Resultsmentioning

confidence: 99%

“…(7,(16)(17)(18) In brief, animals in each study group were placed in the inhalation chamber (40 cm in length, 30 cm in width and…”

Section: Methodsmentioning

confidence: 99%

“…(15) Previous studies have shown that TNF-α and MMP-12 play roles in mice exposed to cigarette smoke. (7,(16)(17)(18) The objective of the present study was to use using immunohistochemical methods in order to investigate the expression of MMP-12, TIMP-2, TNF-α and IL-6 in mice exposed to cigarette smoke.…”

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confidence: 99%

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Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Valença

Pôrto

2008

J. bras. pneumol.

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Objective: Various studies of emphysema involve long-term exposure of animals to cigarette smoke, focusing on the cell type involved in the protease/antiprotease imbalance and on extracellular matrix degradation. In emphysema, increased expression of metalloproteinases is associated with cytokines, and evidence suggests that the matrix metalloproteinase-12 (MMP-12) plays an important role. Our objective was to investigate tissue inhibitor of metalloproteinase-2 (TIMP-2), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) detection by immunohistochemical methods in mouse lung. Methods: Male C57BL/6 mice were exposed 3 times a day to the smoke of 3 cigarettes over a period of 10, 20, 30 or 60 days in an inhalation chamber (groups CS10, CS20, CS30 and CS60, respectively). Controls were exposed to the same conditions in room air. Results: A progressive increase in the number of alveolar macrophages was observed in the bronchoalveolar lavage fluid of the exposed mice. The mean linear intercept, an indicator of alveolar destruction, was greater in all exposed groups when compared to control group. In the CS10, CS20 and CS30 mice, the immunohistochemical index (II) for MMP-12 increased in parallel with a decrease in II for TIMP-2 in the CS10, CS20 and CS30 mice. The II for the cytokines TNF-α and IL-6 was greater in all exposed groups than in the control group. Emphysema, with changes in volume density of collagen and elastic fibers, was observed in the CS60 group. Conclusions: These findings suggest that cigarette smoke induces emphysema with major participation of TNF-α and IL-6 without participation of neutrophils.Keywords: Macrophages, alveolar; Emphysema; Tissue inhibitor of metalloproteinase-2; Interleukin-6. ResumoObjetivo: Muitos estudos sobre enfisema são realizados com exposição de animais à fumaça de cigarro durante um longo tempo, focando o tipo de célula envolvida no desequilíbrio protease/antiprotease e a degradação da matriz extracelular. A expressão aumentada de metaloproteinases no enfisema está associado com citocinas e evidências sugerem um papel importante da metaloproteinase de matriz-12 (MMP-12). Nosso objetivo foi estudar a detecção de inibidor tissular de metaloproteinase-2 (TIMP-2), fator de necrose tumoral alfa (TNF-α) e interleucina-6 (IL-6) por métodos imunohistoquímicos no pulmão de camundongos. Métodos: Camundongos C57BL/6 machos foram expostos 3 vezes ao dia a fumaça de 3 cigarros por um período de 10, 20, 30 ou 60 dias através de uma câmara de inalação (grupos CS10, CS20, CS30 e CS60, respectivamente). O grupo controle foi exposto às mesmas condições ao ar ambiente. Resultados: Nós observamos um aumento progressivo de macrófagos alveolares no lavado broncoalveolar dos grupos expostos. O diâmetro alveolar médio, um indicador de destruição alveolar, aumentou em todos os grupos expostos quando comparado ao grupo controle. O índice imunohistoquímico (II) para MMP-12 aumentou nos grupos CS10, CS20 e CS30 em paralelo a uma redução do II para TIMP-2 nos grupos CS10, CS20 e CS3...

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Section: Resultsmentioning

confidence: 99%

“…(7,(16)(17)(18) In brief, animals in each study group were placed in the inhalation chamber (40 cm in length, 30 cm in width and…”

Section: Methodsmentioning

confidence: 99%

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Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Valença

Pôrto

2008

J. bras. pneumol.

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“…Emphysema is characterized by enlargement of alveolar spaces together with destruction of alveolar walls in the absence of obvious fibrosis [8]. CS causes an inflammatory response in the lower respiratory tract characterized by accumulation of alveolar macrophages associated with a recruitment of fewer neutrophils [9,10]. These activated inflammatory cells release a variety of mediators, including proteases, oxidants and toxic peptides, which can damage lung structures and are believed to be a major cause of the tissue destruction found in emphysema [11].…”

Section: Introductionmentioning

confidence: 99%

“…Reactive oxygen species (ROS) from CS or from inflammatory cells (particularly macrophages and neutrophils) result in several damaging effects in COPD [18], including decreased antiprotease defenses [19] and antioxidants. Many of the adverse effects of smoking may result from oxidative damage to critical biological molecules [9]. Epidemiological evidence indicates that reduced dietary intake of antioxidants may be a determinant of COPD [20]; moreover, population surveys have linked a low dietary intake of the antioxidant vitamins C and E to declining lung function [21].…”

Section: Introductionmentioning

confidence: 99%

Supplementation with vitamins C and E improves mouse lung repair

Valença

Bezerra

Romana‐Souza

et al. 2008

The Journal of Nutritional Biochemistry

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The alleviative effect of flavonol‐type Nrf2 activator rhamnazin from Physalis alkekengi L. var. franchetii (Mast.) Makino on pulmonary disorders

Zhang

et al. 2022

Phytotherapy Research

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Rhamnazin (RN) is a flavonol isolated from the calyxes and fruits of Physalis alkekengi L. var. franchetii (Mast.) Makino, which has been used for treating pulmonary diseases in traditional Chinese medicine. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a therapeutic target for pulmonary diseases. In the present study, the underlying mechanism and pharmacological effect of RN against pulmonary disorders are investigated. Human lung epithelial Beas-2B cell and RAW 264.7 murine macrophagebased cell models, and a cigarette smoke (CS)-induced pulmonary impairment mice model are adopted for investigation in vitro and in vivo. RN is identified to be an Nrf2 activator, which promotes Nrf2 dissociation from Keap1 via reacting with the Cys151 cysteine residue of Keap1, and suppresses Nrf2 ubiquitination. In addition, RN is able to attenuate toxicant-stimulated oxidative stress and inflammatory response in vitro. Importantly, RN significantly relieves CS-induced oxidative insult and inflammation, and RN-induced inhibition of inflammation is related to inhibition of nuclear transcription factor-κB (NF-κB) and induction of cell autophagy. In conclusion, our data indicate that RN is an activator of the Nrf2 pathway and evidently alleviates pulmonary disorders via restricting NF-κB activation and promoting autophagy. RN is a promising candidate for the therapy of pulmonary disorders.

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α-Tocopherol and ascorbic acid supplementation reduced acute lung inflammatory response by cigarette smoke in mouse

Cited by 55 publications

References 44 publications

Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Supplementation with vitamins C and E improves mouse lung repair

The alleviative effect of flavonol‐type Nrf2 activator rhamnazin from Physalis alkekengi L. var. franchetii (Mast.) Makino on pulmonary disorders

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