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Receptor interacting serine/threonine kinase 1 (RIPK1) mediates apoptosis by regulating the classic proapoptotic effectors Bcl-2-associated X protein (Bax) and Bcl-2 homologous antagonist/killer (Bak). Although Bcl-2-related ovarian killer (Bok) is structurally similar to Bak and Bax, it is unclear whether it mediates apoptosis in skeletal muscle ischemia reperfusion (IR) injury. We hypothesized that by regulating Bok-mediated apoptosis, inhibiting RIPK1 with necrostatin-1 would reduce skeletal muscle IR injury.Rats were randomized into four groups: sham (SM), IR, IR treated with necrostatin-1 (NI), or vehicle dimethyl sulfoxide (DI). For the IR group, the right femoral artery was clamped for 4 hours and then reperfused for 4 hours, and for the NI and DI groups, necrostatin-1 (1.65 mg/kg) and the equal volume of dimethyl sulfoxide were intraperitoneally administered prior to IR induction. The structural damage of muscle tissue and protein expression of Bok, Bcl-2, and cleaved caspase-3 were investigated, and apoptotic cells were identified with terminal dUTP nick-end labeling (TUNEL) staining. In vitro, human skeletal muscle cells (HSMCs) were exposed to 6 hours of oxygen-glucose deprivation followed by normoxia for 6 hours to establish an oxygen-glucose deprivation/reoxygenation (OGD/R) model. To determine the role of Bok, cell viability, lactate dehydrogenase (LDH) release, and flow cytometry were examined to demonstrate the effects of necrostatin-1 and Bok knockdown on the OGD/R insult of HSMCs.Necrostatin-1 pretreatment markedly reduced IR-induced muscle damage and RIPK1, Bok, and cleaved caspase-3 expression, whereas upregualted Bcl-2 expression (p0.05). Furthermore, necrostatin-1 prevented mitochondrial damage and decreased TUNEL-positive muscle cells (p0.05). In vitro, HSMCs treated with necrostatin-1 showed reduced Bok expression, increased cell viability, and reduced LDH release in response to OGD/R (p0.05), and Bok knockdown significantly blunted the OGD/R insult in HSMCs.Necrostatin-1 prevents skeletal muscle from IR injury by regulating Bok-mediated apoptosis.

In this work, a novel sodium silicate-modified peanut shell biochar(Si-PSB) was synthesized and used as phosphorus adsorbents. Compared with unmodified biochar(PSB), the adsorption capacity of Si-PSBs increased significantly. The adsorption capacity of 8% sodium silicate solution modified biochar(8%Si-PSB) was 3.9 times higher than that of PSB. The biochar was characterized using scanning electron microscopy(SEM), Fourier transformed infrared(FTIR), and X-ray diffraction(XRD), which confirmed that silica was present on the surface of 8%Si-PSB. The introduction of silica improved the reaction activity of biochar's own metal ions by affecting the morphology of calcium carbonate. The 8%Si-PSB had a good adsorption effect on phosphorus in both acid and alkali environments. Phosphorus adsorption by 8%Si-PSB and PSB was described well by the pseudo-second-order model, and the adsorption capacity after equilibrium fluctuated between 2.79 mg·g

To compare the effect between nebulized and intravenous administration of Shenmai Injection () on pulmonary gas exchange function of patients following tourniquet-induced lower limb ischemia-reperfusion.Thirty-eight patients scheduled for lower extremity surgery were randomized into three groups using the closed envelop method: Shenmai Injection was administered 30 min before tourniquet inflflation by nebulization [0.6 mL/kg in 10 mL normal saline (NS)] in the nebulization group or by intravenous drip (0.6 mL/kg dissolved in 250 mL of 10% glucose) in the intravenous drip group, and equal volume of NS was given intravenously in the NS group; 15 in each group. Arterial blood gases were analyzed, serum levels of malonaldehyde (MDA) and interleukine-6 (IL-6) and interleukine-8 (IL-8) were determined using the method of thiobarbituric acid reaction and enzyme-linked immuno sorbent assay respectively just before tourniquet inflflation (T0), and at 0.5 h (T1), 2 h (T2), 6 h (T3) after tourniquet deflflation.Compared with baselines at T0, MDA levels signifificantly increased at T2, T3 in the NS group and at T3 in the nebulization group, and IL-6 and IL-8 levels were signifificantly increased at T2, T3 in NS, the intravenous drip and the nebulization groups (P0.05). Arterial pressure of oxygen (PaOIntravenous administration of Shenmai Injection provided a better protective effect than nebulization in mitigating pulmonary gas exchange dysfunction in patients following tourniquet-induced limb ischemia-reperfusion.

Aquaporin-1 (AQP1) has involved in fluid transport in diverse pulmonary edema diseases. Our study aimed to explore the dynamic changes of AQP1 in pulmonary water metabolism in rats following traumatic brain injury (TBI) and the protective effect provided by shenmai injection.Sixty male Sprague Dawley rats weighting 280 - 300 g were randomly divided into three groups: the normal control group, the model group and the shenmai injection (SMI) group. One piece skull was taken away without injuring cerebral tissue in normal control group, while rats in model group and SMI group were subject to free fall injury in the cerebral hemisphere. Rats in model group received intraperitoneal normal sodium (15 ml/kg) at one hour post-injury and the same dose of shenmai injection instead in SMI group, respectively. The expression of AQP1 was detected by immunohistochemical analysis and semi-quantitative RT-PCR at 0 hour, 10 hours, 72 hours and 120 hours after TBI. Arterial blood gas analysis and lung wet to dry were also measured.AQP1 was mainly presented in the capillary endothelium and slightly alveolar epithelial cells in three groups, but the expression of AQP1 in the normal control group was positive and tenuous, weakly positive in the model and SMI groups, respectively. Compared with normal control group, AQP1 mRNA levels were down regulated in the model and SMI groups at 10 hours, 72 hours and 120 hours (P0.05). While AQP1 mRNA levels in the SMI group was up-regulated than that in the model group (P0.05). Lung wet to dry weight ratio (W/D) in the model and SMI groups at 10 hours were higher than that in normal control group (P0.05). Compared with normal control group, PaO2 was markedly lower in the model and SMI groups (P0.05), but there were no statistically significant differences between model and SMI groups (P0.05).The decreased AQP1 expression may be involved in the increased lung water content and dysfunction of pulmonary water metabolism following TBI. The treatment with SMI could improve water metabolism by promoting AQP1 expression.