RESUMO
The genus Cuneopsis Simpson, 1900 comprises seven valid species, and Cuneopsis celtiformis (Heude, 1874) is the type species of this genus. Previous phylogenetic studies using complete mitochondrial genomes showed that Cuneopsis was not monophyletic, but the result was hampered by incomplete species sampling and lack of the type species of this genus. In this study, we collected C. celtiformis from the type locality and determined its complete maternal mitochondrial genome. This mitogenome is 15,922 bp in length and contains 14 protein-coding genes (including one F-orf), two rRNA genes, 22 tRNA genes, and 1 putative control region. Our mitochondrial phylogenomic analysis confirms that currently recognized genus Cuneopsis is polyphyletic, and C. celtiformis is the closest to C. heudei with high maximum likelihood bootstrap support value. Comprehensive sampling of all Cuneopsis species is needed for phylogenetic analysis to erect new genera in future studies.
RESUMO
There is very little evidence on the value of administering estrogen in cases of seawater drowning which can induce acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Therefore, this study aimed to investigate whether 17ß-estradiol (E2) treatment can attenuate seawater aspiration-induced ALI in rats. In the experiment, ALI was induced by endotracheal instillation of seawater (4mL/kg) and the rats were then given intraperitoneal injection of E2 (5mg/kg) 20min after seawater instillation. Finally, the changes of arterial blood gases which contained hydrogen ion concentration (pH), arterial oxygen tension (PaO(2)) and arterial carbon dioxide tension (PaCO(2)) were measured and the measurement of extravascular lung water (EVLW) was observed. The pulmonary histological changes were evaluated by hematoxylin-eosin stain. The expression of aquaporins (AQPs) 1, AQP5, and estrogen receptor-ß (ERß) was measured by western blotting and immunohistochemical methods. The results showed that compared with normal saline water, seawater aspiration induced more serious ALI in rats which was markedly alleviated by E2 treatment. Meanwhile, the ERß in lung tissues was activated after E2 administration. The seawater aspiration group also presented with severe pulmonary edema which was paralleled with over expressed AQP1 and AQP5. However, the up-regulation of AQP1 and AQP5 was suppressed by the administration of E2, resulting in an attenuation of lung edema. In conclusion, E2 treatment could effectively attenuate seawater aspiration-induced acute lung injury in rats by the down-regulation of AQP1 and AQP5.
Assuntos
Lesão Pulmonar Aguda/tratamento farmacológico , Estradiol/uso terapêutico , Afogamento Iminente/terapia , Água do Mar/efeitos adversos , Lesão Pulmonar Aguda/metabolismo , Lesão Pulmonar Aguda/patologia , Animais , Aquaporina 1/análise , Aquaporina 5/análise , Dióxido de Carbono/sangue , Receptor beta de Estrogênio/análise , Água Extravascular Pulmonar/efeitos dos fármacos , Pulmão/patologia , Masculino , Ratos , Ratos Sprague-DawleyRESUMO
Relieving pulmonary edema is the key of a successful treatment to seawater drowning. Sodium tanshinone IIA sulfonate (STS) has been observed to reduce lung edema from lipopolysaccharide (LPS)-induced lung injury. In this study the authors investigated whether STS attenuates seawater aspiration-induced acute pulmonary edema, and examined the effects of sodium-potassium adensosine triphosphatase (Na(+),K(+)-ATPase) on it. Seawater was instilled through an endotracheal tube. The anesthetized and spontaneously breathing rats received STS intraperitoneally after seawater aspiration. Pao(2), lung wet-to-dry weight ratio, and pulmonary microvascular permeability were tested. The authors explored the effects of STS on the expression and activity of Na(+),K(+)-ATPase in vivo and in vitro. Additionally, the authors investigated the role of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway in the stimulation of Na(+),K(+)-ATPase by STS. The results showed that STS significantly improved hypoxemia, attenuated lung edema, and alleviated seawater-induced lung injury in vivo. Both in vivo and in vitro, it was observed that STS up-regulated the expression and activity of Na(+),K(+)-ATPase. ERK1/2 inhibitor partially blocked the effects of STS on Na(+),K(+)-ATPase activity in alveolar type II cells following seawater incubation. These results indicated that STS could improve seawater aspiration-induced acute pulmonary edema by up-regulating Na(+),K(+)-ATPase activity, and the ERK1/2 signaling pathway may be involved in it.
Assuntos
Fenantrenos/farmacologia , Edema Pulmonar/tratamento farmacológico , Edema Pulmonar/etiologia , Água do Mar/efeitos adversos , ATPase Trocadora de Sódio-Potássio/metabolismo , Doença Aguda , Animais , Sequência de Bases , Primers do DNA/genética , Medicamentos de Ervas Chinesas/farmacologia , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Pneumonia Aspirativa/tratamento farmacológico , Pneumonia Aspirativa/enzimologia , Pneumonia Aspirativa/etiologia , Pneumonia Aspirativa/genética , Edema Pulmonar/enzimologia , Edema Pulmonar/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , ATPase Trocadora de Sódio-Potássio/genética , Regulação para Cima/efeitos dos fármacosRESUMO
Inflammation takes responsibility for the seawater aspiration-induced lung injury. Tanshinone IIA (TIIA) can protect lipopolysaccharide-induced lung injury in mice through the inhibition of inflammation, but it is not reported whether TIIA have a protective effect on lung injury induced by seawater aspiration. Macrophage migration inhibitory factor (MIF) plays an important role in acute lung injury. In this study, we observed the effect of TIIA on the seawater aspiration-induced lung injury and the role of MIF in it. Seawater was aspirated into trachea of rats to make the lung injury model. TIIA was administered to investigate its beneficial effect on seawater-induced acute lung injury. The results showed that seawater aspiration led to hyoxemia, pulmonary edema, neutrophil infiltration, and lung histopathologic changes, with the elevated MIF expression in the lung tissues and plasma. However, these changes were attenuated by TIIA. In macrophage cells we also demonstrated that TIIA could inhibit MIF expression, nuclear factor κB (NF-κB) activity and release of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) induced by seawater. Besides, pretreatment with (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid (ISO-1), the MIF antagonist, elevated NF-κB and cytokines induced by seawater were also reduced markedly. Furthermore, rMIF treatment alone increased the phosphorylation level of NF-κB and release of cytokines, which was almost abolished by TIIA. Taken together, our results suggested that TIIA exert a protective effect on the seawater aspiration-induced lung injury partly through downregulation of MIF and the subsequent NF-κB activity, as well as expression of IL-6 and TNF-α.
Assuntos
Abietanos/farmacologia , Lesão Pulmonar/prevenção & controle , Fatores Inibidores da Migração de Macrófagos/antagonistas & inibidores , Água do Mar , Animais , Ensaio de Imunoadsorção Enzimática , Lesão Pulmonar/patologia , Masculino , Neutrófilos/patologia , Ratos , Ratos Sprague-DawleyRESUMO
1. Tanshinone IIA (TIIA) is one of the main active components of the Chinese herb, Danshen. In the present study, we investigated the role of apoptosis in seawater exposure-induced acute lung injury (ALI), and explored the effects of TIIA on lung injury, apoptosis, and protein kinase B (Akt) and extracellular signal-regulated protein kinase (ERK) pathways in seawater-challenged rats. The rats were randomly divided into four groups: (i) naive group, no drug was given; (ii) TIIA control group, TIIA (50 mg/kg) was given intraperitoneally; (iii) seawater (SW) group, seawater (4 mL/kg) was given; and (iv) TIIA/SW group, TIIA (50 mg/kg) was injected intraperitoneally 10 min after seawater instillation. 2. The results showed that TIIA treatment significantly improved seawater exposure-induced lung histopathological changes, alleviated the decrease in PaO(2) , and reduced lung oedema, vascular leakage and cell infiltration. As shown by terminal deoxynucleotidyl transferase-mediated nick end labelling (TUNEL) assay, seawater exposure induced apoptosis in lung tissue cells. Furthermore, seawater exposure also changed apoptosis-related factors Bcl-2 and caspase-3, and caused a reduction in the activation of Akt and ERK1/2 pathways. Furthermore, TIIA treatment decreased the number of apoptotic cells, reversed changes in Bcl-2 and caspase-3, and upregulated the activation of Akt and ERK1/2 in seawater-challenged rats. 3. In conclusion, the data suggest that apoptosis might play an important role in seawater exposure-induced lung injury and that TIIA could significantly attenuate the severity of ALI and apoptosis in seawater-challenged rats, which is possibly through modulation of Akt and ERK1/2 pathways.
Assuntos
Abietanos/farmacologia , Lesão Pulmonar Aguda/tratamento farmacológico , Apoptose/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Lesão Pulmonar Aguda/enzimologia , Lesão Pulmonar Aguda/patologia , Animais , Apoptose/fisiologia , Caspase 3/genética , Caspase 3/metabolismo , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Oxigênio/sangue , Oxigênio/metabolismo , Pressão Parcial , Ratos , Ratos Sprague-Dawley , Água do Mar , Proteína de Morte Celular Associada a bcl/genética , Proteína de Morte Celular Associada a bcl/metabolismoRESUMO
OBJECTIVE: To explore the effects of tanshinone IIA on the activity of aquaporin-5 (AQP5) in human alveolar epithelial cells (A549) after seawater exposure and its possible mechanism. METHODS: Routinely cultured A549 cells were divided into different groups according to different content of seawater: blank control group, 15%, 25%, 50%, 75%, 100% seawater groups; they were divided into different groups according to the duration of exposure to 25% seawater: blank control group, 1, 4, 8 hours groups; they were also divided into different groups according to concentration of tanshinone IIA and exposed to seawater for 4 hours: blank control group, 25% seawater group, 25, 50, 75, 100 µg/ml tanshinone IIA intervention groups. The expressions of AQP5 were respectively assayed by Western blotting and immunohistochemistry. RESULTS: The results of Western blotting showed that the expressions of AQP5 were remarkably higher at 8 hours of exposure to seawater in 25% and 50% seawater groups than those in blank control group (1.053±0.231, 1.116±0.316 vs. 0.101±0.081, both P<0.05); the expression of AQP5 in 1-hour group showed a slight increase compared with blank control group (0.306±0.125 vs. 0.288±0.098, P>0.05), that in 4-hour group was increased significantly (1.423±0.377, P<0.01), and in 8-hour group (1.507±0.461) it was slightly higher than that in 4-hour group without statistical significance. The AQP5 expression was significantly lower in tanshinone IIA 25 µg/ml and 50 µg/ml intervention groups than that in 25% seawater group (0.580±0.186, 0.499±0.172 vs. 1.013±0.287, both P<0.05). Immuno-histochemistry showed that the expression of AQP5 was markedly up-regulated after A549 cells were stimulated with 25% seawater for 4 hours as compared with blank control group (7.21±0.78 vs. 0.41±0.07, P<0.01), but intervention of tanshinone IIA significantly inhibited the up-regulation of AQP5 expression (3.02±0.23) induced by 25% seawater (P<0.05). CONCLUSION: The experimental results showed that tanshinone IIA is innocuous to A549 at a dosage of 25 µg/ml, and it can decrease the overexpression of AQP5 induced by seawater.