Complete maternal mitochondrial genome of the freshwater mussel Cuneopsis celtiformis (Bivalvia: Unionidae).

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.

Sodium tanshinone iia sulfonate attenuates seawater aspiration-induced acute pulmonary edema by up-regulating Na(+),K(+)-ATPase activity.

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.

Tanshinone IIA attenuates seawater aspiration-induced lung injury by inhibiting macrophage migration inhibitory factor.

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.

Tanshinone IIA suppresses lung injury and apoptosis, and modulates protein kinase B and extracellular signal-regulated protein kinase pathways in rats challenged with seawater exposure.

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.

[Effect of sulfonic tanshinone sodium injection on the expression and activity of aquaporin-5 of human alveolar epithelial cells after seawater exposure].

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.