Acute respiratory distress syndrome (ARDS) is a common respiratory emergency, but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures. Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS, but the application of hydrogen has flammable and explosive safety concerns. Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance, thus improving ARDS in patients and animal models. Coral calcium hydrogenation (CCH) is a new solid molecular hydrogen carrier prepared from coral calcium (CC). Whether and how CCH affects acute lung injury in ARDS remains unstudied. In this study, we observed the therapeutic effect of CCH on lipopolysaccharide (LPS) induced acute lung injury in ARDS mice. The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable, demonstrating a significant improvement compared to the untreated ARDS model group. CCH treatment significantly reduced pulmonary hemorrhage and edema, and improved pulmonary function and local microcirculation in ARDS mice. CCH promoted mitochondrial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2 (Trx2), improved lung mitochondrial dysfunction induced by LPS, and reduced oxidative stress damage. The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

Objective To investigate the common initial clinical presentations of primary Sj(o)gren's syndrome (pSS) with pulmonary complications,and to explore the differences between patients with extraglandular manifestations at disease onset (EGM) and those with glandular manifestations at disease onset (GM).Methods A total of 1 341 hospitalized SS patients from 2003 to 2012 were retrospectively reviewed.Of them,102 hospitalized patients with pSS'associated lung disease were analyzed and included.Case control study was performed to explore the differences between the EGM group and the GM group.Results Fifty-one percent of patients were presented with EGM at onset,with significantly shorter disease duration [36 (12,156) m vs 102 (48,159) m,x2=-2.41,P=0.016].Although the mean diagnose time was similiar,only 4％ of the EGM group could be confirmed the pSS diagnose at onset,which was significantly less frequently than that of the GM group (34％,22=15.29,P＜0.01).Case control study revealed that hyperglobulinemia,elevated RF titers and anti-SSA and/or anti-SSB test positive were less predominant in the EGM group [IgG 16(12,21) g/L vs 21 (15,28) g/L,x2=-2.15,P=0.032;22 (20,171) U/ml vs 104 (20,238) U/ml,x2=-l.98,P=0.048;33％ vs 72％,x2=15.78,P＜0.01].The predicted value of TLC and FVC were lower [(87±23)％ vs (97±20)％,x2=-1.96,P=0.050;(8±28)％ vs (100±27)％,x2=-1.70,P=0.089] and HRCT score was higher in EMG group [12(88,15) vs 8(5,13),x2=-1.82,P=0.070].Conclusion EMG at onset is the common initial manifestation of pSS'associated lung involvement.Pulmonary complication is more progressively and severe than those with MG at onset.Anti'SSA positive,elevated RF titer and hyperglobulinemia are not predominant for patients with EMG at onset.

ObjectiveToinvestigatetheprotectiveeffectandmechanismofscutelarincombinedwith paeoniflorin after permanent cerebral ischemia in rats. Methods Forty-eight adult male SD rats w ere randomly divided into four groups: sham-operation, cerebral ischemia, scutelarin+ paeoniflorin, and cyclopamine (n=12 in each group). A model of permanent middle cerebral artery occlusion w as induced by suture method. The intraperitoneal injection of cyclopamine 6 mg/kg, a specific inhibitor of sonic hedgehog (SHH) pathw ay, at 15 min before ischemia in the cyclopamine group, w hile other groups w ere intraperitoneal y injected an equal volume of saline. At 0 hour and 3 hours after ischemia, the scutel arin+paeoniflorin group and cyclopamine group w ere intraperitoneal y injected scutel arin ( 20 mg/kg ) and paeoniflorin (30 mg/kg), while other groups were intraperitonealy injected an equal volume of saline. Neurological deficit scores w ere performed at 24 hours after ischemia, and then the rats w ere decapitated. The cerebral infarct volume w as measured by using 2,3,5-triphenyltetrazolium chloride (TTC) staining. Real-time fluorescent quantitative polymerase chain reaction and Western blotting w ere used respectively to detect the expression levels of SHH, Patched-1, Gli-1 mRNAs and proteins in the ischemic cortex. Results The neurological deficit scores in the cerebral ischemia group, scutel arin+paeoniflorin group, and cyclopamine group w ere 3.33 ±0.52, 1.50 ±0.55, and 3.67 ±0.52, respectively. The neurological deficit score in the scutel arin+paeoniflorin group w as significantly low er than that in the cerebral ischemia group ( P<0.05), and the neurological deficit score in the cyclopamine group w as significantly higher than that in the scutelarin+paeoniflorin group ( P<0.05). The infarct volume percentage in the cerebral ischemia group, scutelarin+paeoniflorin group, and cyclopamine group were 31.77%±1.19%, 22.94%±2.65%, and 35.53%±0.20%, respectively. The infarct volume in the scutel arin+paeoniflorin group w as significantly less than that in the cerebral ischemia group ( P<0.05), and the infarct volume in the cyclopamine group was significantly larger than that of the scutelarin+paeoniflorin group (P<0.05). The expression levels of SHH, Patched-1, Gli-1 mRNAs and proteins in the cerebral ischemia group, scutelarin+paeoniflorin group, and cyclopamine group w ere significantly higher than those in the sham -operation group (al P<0.05). The expression levels of SHH, Patched-1, Gli-1 mRNAs and proteins in the scutelarin+paeoniflorin group were significantly higher than those in the in the cerebral ischemia group (al P<0.05), and the expression levels of Gli-1 mRNA and protein in the cyclopamine group were significantly lower than those in the scutelarin+paeoniflorin group ( al P<0.05 ). Conclusions The scutel arin combined w ith paeoniflorin has certain protective effect on focal cerebral ischemia injury in rats. Its mechanism is associated w ith the activation of SHH signaling pathw ay.