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This study analyzed the quality markers(Q-markers) of Yuquan Capsules(YQC) based on serum pharmacochemistry of Chinese medicine and detected the components and metabolites of YQC absorbed into the blood by UPLC-Q-TOF-MS and UNIFI systems. As a result, 32 components of YQC were detected, including 17 prototype components and 15 metabolized components. Among them, 12 prototype components(ginsenoside Rh_2, genistein, formononetin, puerarin, daidzein, schizandrin A, schizandrin B, schizandrin C, schizandrol A, schizandrol B, gomisin D, and ononin) and 12 metabolized components(ginsenoside Rg_1, ginsenoside Rg_2, ginsenoside Rg_3, ginsenoside Ro, 3'-methoxypuerarin, daidzin, astragaloside Ⅱ, astragaloside Ⅳ, glycyrrhizic acid, liquiritigenin, isoliquiritin, and verbascoside) showed inhibitory effects and pharmacological activities against diabetes, and these 24 blood-entering components against diabetes were identified as Q-markers of YQC.
Subject(s)
Capsules , Chromatography, High Pressure Liquid , Drugs, Chinese Herbal/pharmacology , Ginsenosides/analysis , Medicine, Chinese Traditional , Serum/chemistryABSTRACT
OBJECTIVE@#To study whether sevoflurane pretreatment inhibits the myocardial apoptosis caused by hypoxia reoxygenation through AMPK pathway.@*METHODS@#H9c2 myocardial cell lines were cultured and divided into control group (C group), hypoxia reoxygenation group (H/R group), sevoflurane pretreatment + hypoxia reoxygenation group (SP group) and sevoflurane combined with Compound C pretreatment + hypoxia reoxygenation group (ComC group), and the cell proliferation activity and apoptosis rate, myocardial enzyme levels in culture medium as well as the expression of apoptosis genes and p-AMPK in cells were determined.@*RESULTS@#p-AMPK expression in cells of H/R group was significantly lower than that of C group, SP group was significantly higher than that of H/R group; cell proliferation activity value and Bcl-2 expression in cells of H/R group were significantly lower than those of C group, SP group were significantly higher than those of H/R group, ComC group were significantly lower than those of SP group; apoptosis rate, LDH, CK and AST levels as well as the Bax and Caspase-3 expression in cells of H/R group were significantly higher than those of C group, SP group were significantly lower than those of H/R group, ComC group were significantly higher than those of SP group.@*CONCLUSIONS@#Sevoflurane pretreatment can activate AMPK signaling pathway to inhibit the myocardial apoptosis caused by hypoxia reoxygenation.
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Objective To study whether sevoflurane pretreatment inhibits the myocardial apoptosis caused by hypoxia reoxygenation through AMPK pathway. Methods H9c2 myocardial cell lines were cultured and divided into control group (C group), hypoxia reoxygenation group (H/R group), sevoflurane pretreatment + hypoxia reoxygenation group (SP group) and sevoflurane combined with Compound C pretreatment + hypoxia reoxygenation group (ComC group), and the cell proliferation activity and apoptosis rate, myocardial enzyme levels in culture medium as well as the expression of apoptosis genes and p-AMPK in cells were determined. Results p-AMPK expression in cells of H/R group was significantly lower than that of C group, SP group was significantly higher than that of H/R group; cell proliferation activity value and Bcl-2 expression in cells of H/R group were significantly lower than those of C group, SP group were significantly higher than those of H/R group, ComC group were significantly lower than those of SP group; apoptosis rate, LDH, CK and AST levels as well as the Bax and Caspase-3 expression in cells of H/R group were significantly higher than those of C group, SP group were significantly lower than those of H/R group, ComC group were significantly higher than those of SP group. Conclusions Sevoflurane pretreatment can activate AMPK signaling pathway to inhibit the myocardial apoptosis caused by hypoxia reoxygenation.
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Objective To investigate the morphological changes of different types of axonal injury in acute stage in rat brain with diffuse axonal injury(DAD caused by combined head injuries,and explore their relevant injury mechanisms. Methods SD rats were randomized into experimental (n=16)and normal control(=8)groups.According to the different injury times(6,24 h),the experimental group was equally divided into two subgroups(n=8).A new experimental facility was employed to induce DAI in rats.HE staining was conducted in different time points in the acute stage.Immunofluorescence assay was performed to detect the expressions of antibodies to β-Amyloid precursor protein(β-APP)and antibodies to neurofilament-68(NF-68)and electron microscope was also introduced to investigate the changes of axonemal ultrastructure.Results All injured rats experienced behavioral suppression:the coma in the experimental group was significantly prolonged as compared to that in the normal control group(P<0.05).Immunofluorescence assay for antibodies to β-APP and NF-68 revealed two distinct types of axonal injuly: β-APP confined to focal spheroidal axonal swellings and axonal retraction bulbs;while NF-68 Was only found within thin and elongate axonal segments. Electron microscope also demonstrated two different types of ultrastructure of axonal injury. Conclusion Impaired axonal transport and neurofilament compaction can occur independently in the process of axonal injury with different morphological changes.Multiple immunocytochemical approaches can help to fully assess the overall axonai response to traumatic brain injury.
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Objective To investigate the influence of nerve growth factor (NGF) on the level of plasma creatine kinase BB (CK-BB) and its clinical effect in patients with severe craniocerebral trauma. Methods Eighty patients with severe craniocerebral trauma (GCS≤8) were randomly assigned to NGF-treated (n=40) and control (n=40) groups. Conventional therapy was performed on these patients and NGF was added into the NGF-treated group. The level of plasma CK-BB in these patients was measured; the clinical prognosis of the patients was evaluated based on the GOS scores 6 months after severe craniocerebral trauma; the condition of regained consciousness was compared between the 2 groups. Results Plasma CK-BB in the NGF-treated group was significantly lower than that in the control group (P<0.05); the recovery rate in the NGF-treated group (24/40) was significantly higher than that in the control group (11/40); the consciousness regained within i month was found in 32 patients in the NGF-treated group but only 18 of that was noted in the control group (P<0.05); NGF-treated group (12.43±6.25) showed a significantly shorter time that consciousness was regained as compared with the control group (15.96±7.58). Conclusion NGF can decrease the level of plasma CK-BB, shorten coma time and improve life quality in patients with severe craniocerebral trauma. Application ofNGF, a safe and effective treatment method, provides a new potential therapeutic strategy for patients with CNS injury.