Analysis on Evolution of Ancient Documents of Xiehuangsan / 中国实验方剂学杂志

Xiehuangsan， derived from QIAN Yi's Key to Therapeutics of Children's Diseases， consists of 5 medicines， namely Gypsum Fibrosum，Gardeniae Fructus，Saposhnikoviae Radix，Pogostemonis Herba and Glycyrrhizae Radix et Rhizoma. It is used to treat children with spleen heat and tongue scratching. With the clinical use of later generations of physicians，the scope of diseases and syndromes of this prescription was gradually expanded，including aphthous bad breath，dry lips，yellow eyes，and sweet mouth. Modern doctors used this prescription to treat children with anorexia，constipation，allergic purpura，tic disorder， and other diseases. At present，more and more attention has been paid to the research of classical famous prescriptions. At the same time，the application of classical famous prescriptions of traditional Chinese medicine（TCM） must be researched and verified in ancient literature. Therefore，it has become important contents in the study of classic prescriptions that researching the source of prescriptions from the ancient books，combing and analyzing literature，and studying the evolution rules of indications，preparations，methods of administration and taboos.The author searched a variety of ancient Chinese medicine databases and collected the relevant documents related to Xiehuangsan in ancient medical books. A total of 242 pieces of relevant ancient document data were obtained，involving 131 types of ancient Chinese medicine books. Through combing the relevant records of historical documents，this paper analyzes and researches the historical evolution of Xiehuangsan，the source and composition of the prescriptions，the indications，the dosage，the textual research of Chinese herbal medicine and the determination of the basis，and the method of prescription preparation and administration，etc. The historical changes of Xiehuangsan and its internal relations are expected to provide literature references and theoretical basis for the modern development and research of Xiehuangsan.

Portal vein arterialization for acute hepatic failure in rats / 中国组织工程研究

BACKGROUND: Partial portal vein arterialization (PPVA) can slow the progression of liver failure by increasing the blood supply. OBJECTIVE: To explore the effects of PPVA on the liver function and pathological changes in a rat model of liver failure.METHODS: Totally 130 Sprague-Dawley rats were randomized into three groups: PPVA group (n=50) underwent left nephrectomy, the PPVA model was established by sleeve suturing and cuff technology, and then D-galactosamine was intraperitoneally administered at the dose of 1 300 mg/kg to induce acute liver failure; liver failure group (n=50) underwent left nephrectomy, the portal vein was dissociated, ligated for 16 minutes and then mobilized, and D-galactosamine was intraperitoneally administered at the dose of 1 300 mg/kg to induce acute liver failure after abdominal closure; control group (n=30) received left nephrectomy, the portal vein was ligated for 16 minutes and then mobilized, and same volume of normal saline was intraperitoneally administered after abdominal closure. The serological and pathological changes of the liver tissue were observed at 12, 24, 36, 48 and 72 postoperative hours. RESULTS AND CONCLUSION: Animal models (n=30 per group) were made successfully, the survival rate was 70% and 53%, respectively, and there was a significant difference between two groups after modeling (P < 0.05). The survival rate in the control group was 100% at 72 postoperative hours. The serum levels of glutamic-oxalacetic transaminease, alanineaminotranferase, interleukin 6, tumor necrosis factor α, and endotoxin in the portal vein in the control group were significantly lower than those in the other two groups at different time points postoperatively (P < 0.05). In the PVA group, the serum levels of glutamic-oxalacetic transaminease and alanineaminotranferase at postoperative different time points postoperatively, the serum levels of total bilrubin, interleukin 6, tumor necrosis factor α, and endotoxin level in the portal vein at 24-72 postoperative hours, and albumin at 36-72 postoperative hours were significantly lower than those in the liver failure group (P < 0.05). At 72 postoperative hours, the liver structure was complete in the control group, hepatic lobules were damaged accompanied with abundant inflammatory cell infiltration in the liver failure group and the pathological lesions were improved in the PVA group. To conclude, PVA can improve liver function and slow the progression of liver failure to certain extents.

Study on allergy of Astragaloside injection / 药物评价研究

Objective To evaluate the hypersusceptibility of Astragaloside injection on animal,and provide reference for clinical use with active systemic anaphylaxis (ASA),passive cutaneous anaphylaxis (PCA) and determination of serum sample titer.Methods ASA:Guinea pigs was ip with 0.4,1.6 mg/kg Astragaloside injection five times every other day.On the eleventh day after the last administration,the test substance was quickly injected to fore limb vein,and animal allergy symptoms were observed within 30 min.PCA:Astragaloside injection was ip injected to rats five times every other day and antiserum was collected.The antiserum was appropriately diluted,and sc injected to another group rats for passive sensitization.About 48 hours later,Astragaloside was quickly iv to rats,and the skin allergy was observed.Meanwhile,the antibody titer of the antiserum was determined.Results ASA:Astragaloside injection of 0.4,1.6 mg/kg in guinea pigs did not show any allergic reaction,that is,ASA was negative;PCA:Astragaloside injection of 0.5,2.0 mg/kg in rats did not show any allergic reaction,and Astragaloside specific antibodies were not determined in serum samples.That is,PCA was negative.Conclusion The results of ASA and PCA were negative in the experimental dose,and there was no specific antibody against Astragaloside in the serum prepared by PCA,which indicated that the possibility of hypersensitivity reaction was weak in clinical use.

Study on allergy of Astragaloside injection / 药物评价研究

Objective To evaluate the hypersusceptibility of Astragaloside injection on animal,and provide reference for clinical use with active systemic anaphylaxis (ASA),passive cutaneous anaphylaxis (PCA) and determination of serum sample titer.Methods ASA:Guinea pigs was ip with 0.4,1.6 mg/kg Astragaloside injection five times every other day.On the eleventh day after the last administration,the test substance was quickly injected to fore limb vein,and animal allergy symptoms were observed within 30 min.PCA:Astragaloside injection was ip injected to rats five times every other day and antiserum was collected.The antiserum was appropriately diluted,and sc injected to another group rats for passive sensitization.About 48 hours later,Astragaloside was quickly iv to rats,and the skin allergy was observed.Meanwhile,the antibody titer of the antiserum was determined.Results ASA:Astragaloside injection of 0.4,1.6 mg/kg in guinea pigs did not show any allergic reaction,that is,ASA was negative;PCA:Astragaloside injection of 0.5,2.0 mg/kg in rats did not show any allergic reaction,and Astragaloside specific antibodies were not determined in serum samples.That is,PCA was negative.Conclusion The results of ASA and PCA were negative in the experimental dose,and there was no specific antibody against Astragaloside in the serum prepared by PCA,which indicated that the possibility of hypersensitivity reaction was weak in clinical use.

Progress in research of the structural optimization of natural product-like Garcinia caged xanthones / 药学学报

Designing of natural product-like compounds using natural products as template structures is an important strategy for the discovery of new drugs. Gambogic acid (GA), which is a Garcinia natural product with a unique caged xanthone scaffold, inhibits potent antitumor activity both in vitro and in vivo. This review summarized the researches on the identification of the antitumor pharmacophore of GA, and the design, structural optimization and structure-activity relationship (SAR) of natural product-like caged xanthones based on it.

Prelimary exploration on Chinese medicine syndrome type distribution in patients with polycystic ovary syndrome / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the Chinese medicine syndrome type distribution in patients with polycystic ovary syndrome (PCOS) and its relationship with sexual hormones.</p><p><b>METHODS</b>Chinese medicine syndrome types of 212 PCOS patients were differentiated and sorted by adopting fuzzy mean C clustering method, and their relationship with the indices of sexual hormones detected on the 3rd to 5th day of menstrual cycle was analyzed, with the values got from 20 healthy women for controls.</p><p><b>RESULTS</b>Intermingling syndromes were commonly seen in PCOS patients. Shen-deficiency syndrome (presented in 64 patients) and Gan-qi stagnancy syndrome (61 patients) were the dominance, accounting for 30.2% and 28.8% respectively, significantly higher than that of other syndromes (P < 0.05), which were Pi-deficiency syndrome (41 patients, 19.3%), phlegm-dampness syndrome (33 patients, 15.6%) and blood stasis syndrome (13 patients, 6.1%). Levels of estradiol (E2), testosterone (T), luteinzing hormone (LH), dehydroiso-androsterone (DHEA-S) and prolactin (PRL) were higher, while the level of sexual hormone binding protein (SHBG) was lower in PCOS patients than those in control, follicular stimulating hormone (FSH) level in patients of Shen-deficiency syndrome and phlegm-dampness syndrome was high than that in control (P < 0.05 and P < 0.01). However, no significant differences were found in comparing the various sexual endocrinal indices between patients with different syndrome types (P > 0.05). Besides, the level of PRL was positively correlated with LH and E2 levels in patients.</p><p><b>CONCLUSION</b>Chinese medicine syndromes presented in patients with PCOS are mostly intermingling, Shen-deficiency and Gan-stagnancy are the basic syndromes, and there is some correlation between syndrome type and sexual hormone levels.</p>

Treatment of non-alcoholic fatty liver disease by Qianggan Capsule / 中国结合医学杂志

<p><b>OBJECTIVE</b>To observe the therapeutic effect and safety of Qianggan Capsule (QGC) in treating non-alcoholic fatty liver disease (NAFLD), using polyene phosphatidylcholine capsule (PPC) as a reference.</p><p><b>METHODS</b>Eighty-eight patients with NAFLD were randomly assigned to two groups, 45 in the treatment group treated with QGC and 43 in the control group treated with PPC. The course of treatment lasted for 6 months. Changes in liver function, blood lipids, and iconographic indexes before and after treatment were observed, and clinical efficacy was evaluated.</p><p><b>RESULTS</b>In the treatment group, alanine aminotransferase (ALT) was lowered significantly from 56.02 + or - 32.59 IU/L before treatment to 38.27 + or - 22.68 IU/L after treatment, and CT liver/spleen ratio significantly increased from 0.69 + or - 0.18 to 0.91 + or - 0.25, showing statistical significance (P<0.05); in contrast, the corresponding changes of the two indexes in the control group were 56.56 + or - 26.33 IU/L to 49.67 + or - 26.22 IU/L, and 0.66 + or - 0.20 to 0.75 + or - 0.24, respectively, the pre-post treatment difference showing insignificant difference (P>0.05). No severe adverse reactions occurred during the whole treatment course.</p><p><b>CONCLUSION</b>QGC is an effective and safe remedy for the treatment of NAFLD.</p>

Heat shock protein 27 attenuated doxorubicin-induced myocardial damage by reducing cardiomyocyte apoptosis, mitochondria damage and protein carbonylation / 中华心血管病杂志

<p><b>OBJECTIVE</b>Oxidative stress and apoptosis play a critical role in the pathogenesis of congestive heart failure (CHF) induced by doxorubicin (Dox) or ischemia/reperfusion. Heat shock protein 27 (Hsp27) could reduce oxidative stress induced apoptosis in various cell types in vitro and attenuate ischemia/reperfusion induced cardiac dysfunction in isolated perfused mouse heart. In this study, we investigated the impact of Hsp27 overexpression on oxidative stress and apoptosis in Dox-induced mice cardiac dysfunction model.</p><p><b>METHODS</b>Both Hsp27 transgenic mice (TG) and wild type littermates (WT) received a single dosage of Dox (25 mg/kg IP) or saline. On day 3, histological examinations (Paraffin section and HE staining, mitochondria ultrastructure), in situ cardiomyocytes apoptosis assay (TUNEL, immunohistochemistry against alpha-actinin for cardiomyocytes, hoechst33342 for nuclei staining), protein oxidative damage assay (immunoblot against DNP) were performed on cardiac tissue samples. Pleural effusion and histological changes of heart and lung were examined in dead mice.</p><p><b>RESULTS</b>(1) Significant pleural effusion, pulmonary congestion, alveoli collapse and extravasated red blood cells were observed in all died mice. (2) Pronounced cardiomyocyte damages and inhomogeneous HE staining were observed in almost all dead mice except for one TG mouse died at day 4 which showed homogeneous HE staining and only slightly cardiomyocyte damages. (3) Cardiac fibrosis was presented in WT mice but not in TG mice. (4) Dox-induced cardiomyocyte apoptosis and protein carbonylation were significantly attenuated in TG mice compared those in WT mice. (5) Severity of Dox-induced mitochondria damage including increased density, swollen cristae and loss of cristae definition was significantly reduced in TG mice compared to that in WT mice were seen in all the examined myocytes of the LV myocardium samples of Dox-treated mice.</p><p><b>CONCLUSION</b>Hsp27 could attenuate Dox-induced myocardial damage by reducing cardiomyocyte apoptosis, mitochondria damage and protein carbonylation.</p>

Overexpression of heat shock protein 27 reduces mortality and attenuates cardiac dysfunction induced by doxorubicin in a transgenic mouse model / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the effects of heat shock protein 27 (Hsp27) overexpression on doxorubicin (Dox) induced mortality and cardiac dysfunction in a transgenic (TG) mouse model.</p><p><b>METHODS</b>A linear DNA constituted of alpha-myosin heavy chain (alpha-MHC) promoter, human Hsp27cDNA and poly A was microinjected into fertilized eggs to generate transgenic mice and mice containing the transgene were identified by polymerase chain reaction and independent transgenic lines were established. Following successful transmission, tissues including heart, lung, liver, brain, skeleton muscle, spleen and kidney were screened by Western blot to confirm the cardiac specific expression of the transgene. TG and wild type littermates (WT) received a single dosage of Dox injection (25 mg/kg IP) or saline injection and observed for 5 days. Mice mortality was noticed and left ventricular (LV) hemodynamics were measured at day 5 in surviving mice. Cardiomyocyte apoptosis was evaluated by TUNEL assay at day 3 post Dox or saline injections in a separate group.</p><p><b>RESULTS</b>Three independent transgenic lines were generated, and all of them expressed cardiac specific Hsp27. Five days mortality was significantly reduced in TG group than that in WT group post Dox (P < 0.01), Dox induced cardiac dysfunction and cardiomyocyte apoptosis were also significantly attenuated in TG mice compared to WT mice (P < 0.05).</p><p><b>CONCLUSION</b>Overexpression of Hsp27 reduced mortality, attenuated left ventricular dysfunction and cardiomyocyte apoptosis induced by Dox in a transgenic mouse model.</p>

Heat shock protein 27 regulates oxidative stress-induced apoptosis in cardiomyocytes: mechanisms via reactive oxygen species generation and Akt activation / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Increased reactive oxygen species (ROS) formation, which in turn promotes cardiomyocytes apoptosis, is associated with the pathogenesis and progression of various cardiac diseases such as ischemia and heart failure. Recent studies have shown that over expression of heat shock protein 27 (Hsp27) confers resistance to cardiac ischemia/reperfusion injury. However, not much is known about the regulation of myocyte survival by Hsp27.</p><p><b>METHODS</b>The rat cardiac cell line H9c2, with a stable overexpression of Hsp27, was established, with empty vector transfected H9c2 cells as controls. Following the cells challenged by Hydrogen Peroxide (H2O2), lactate dehydrogenase (LDH) release, apoptosis, intracellular ROS, cell morphology, mitochondrial transmembrane potential and the activation of serine/threonine kinase Akt were determined.</p><p><b>RESULTS</b>Along with marked suppression of H2O2-induced injury by Hsp27 overexpression in H9c2 cells, ROS generation and the loss of mitochondrial membrane potential were also significantly depressed. Furthermore, augmented Akt activation was observed in Hsp27 overexpressed H9c2 cells following H2O2 exposure.</p><p><b>CONCLUSIONS</b>Hsp27 inhibits oxidative stress-induced H9c2 damage and inhibition of ROS generation and the augmentation of Akt activation may be involved in the protective signaling.</p>

Application of UMSARS-Ⅰ in evaluation of illness severity in patients with multiple system atrophy / 上海第二医科大学学报

Objective To investigate the reliability of a novel rating scale, unified multiple system atrophy rating scale, section Ⅰ(UMSARS-Ⅰ) in the evaluation of illness severity in patients with multiple system atrophy (MSA). Methods A retrospective analysis and a prospective follow-up study were conducted by using UMSARS-Ⅰ in 46 patients with MSA, and the Schwab and England scale was employed and illness severity was graded. The reliability, validity and sensitivity to change of UMSARS-Ⅰ in evaluating the illness severity of MSA were estimated. Results UMSARS-Ⅰ enjoyed high internal consistency (standard Crohnbach's ?=0.88) and sound content, criterion-related, construct and discriminant validity in the evaluation of illness severity of MSA, and a moderate sensiti-vity to change was found(effect size=0.61). Conclusion UMSARS-Ⅰ is a reliable and multidimensional semi-quantitative scale in the measurement of severity and progression of impairment in MSA.

Generation of Transgenic Mice with Cardiac-specific Overexpressing Heat Shock Protein 27 / 中国生物工程杂志

Objective:Increased reactive oxygen species (ROS) formation and by which in turn promotes cardiomyocytes apoptosis is associated with the pathogenesis and progression of various cardiac diseases. Small heat shock protein 27(Hsp27) could protect different cells from oxidative damage. By using tissue nonspecific overexpression Hsp 27 transgenic model, other investigators demonstrated that Hsp27 suppressed successfully kainate-induced seizures and hippocampal cell death in intact transgenic mice, and attenuated mimic ischemia/reperfusion injury in Langendorff-perfused isolated mice heart. As there are complicated and long distance neuro-humoral regulation associated with the development of cardiac diseases, it is better to choose a cardiac-specific overexpression transgenic model to study the effects of Hsp27 in hearts in vivo.Methods:A cDNA encoding human Hsp27 was subcloned into pBSII-SK+ containing the ?-myosin heavy chain (?-MHC) promoter (generously provided by Dr. J. Robbins, Children’s Hospital of Cincinnati, Ohio). BamHI-digested linear transgene consistent with the ?-MHC promoter, Hsp27 cDNA, and poly (A) of human growth hormone (hGH) was microinjected into the fertilized eggs from CBA/BL6 mice. Mice containing the transgene were identified by polymerase chain reaction. Founders revealed by this screening were used to establish independent transgenic lines. Following successful transmission, a range of tissues including heart, lung, liver, brain, skeleton muscle, spleen and kidney was screened by Western blot to confirm the cardiac specific expression of the transgene. Results and Discussion:Transgenic mice expressed Hsp27 under the control of a-MHC promoter. Cardiac tissues from independent TG line expressed abundant Hsp27, and as expected, Hsp27 expressed in cardiac tissues only, whereas none in liver, spleen, lung, kidney, brain and skeleton muscle. Surprisingly, Hsp25, the endogenous isoform of Hsp27 in murine, was downregulated by Hsp27 overexpression (data not shown), which is in contrast to the result of Hollander’s [1]. It needs to determine in future whether Hsp27 expression profile in heart could exert any effect on the regulation of Hsp25.Conclusion: The TG mice overexpression human Hsp27 specifically in the heart by using ?MHC- promotor were created. All TG mice expressed Hsp27 abundantly and cardiac-specifically. To our knowledge, it is the first report of creation of transgenic mice which overexpressing Hsp27 cardiac specifically. This current model suggests that the Hsp27 cardiac-specific over-expression of transgenic mouse remains a robust genetic tool for dissecting molecular and genetic events involving Hsp27, which could be a therapeutic target in heart failure.

Overexpression of heat-shock proteins B1 protected rat cardiac cell line H9c2 from H_2O_2-induced oxidative damage / 中华老年医学杂志

Objective To determine the effect of mitochondria on the protection of heat-shock proteins B1(HSPB1) from oxidative damage in rat cardiac cell.Methods HSPB1 gene-transfected rat cardiomyocytes cell line H9c2 (HSPB1 H9c2) and empty vector transfected H9c2 (control) were established,and treated by 0-1000?mol/L H_2O_2 for 2h.And then the cell morphology, mitochondrial membrane potential and endogenous reactive oxygen species (ROS) were detected. Results (1)HSPB1 inhibited the morphological changes induced by H_2O_2 markedly.(2)HSPB1 inhibited the loss of mitochondrial membrane potential induced by H_2O_2.Following the stimulation of 0,75,150,300,500,1000?mol/L H_2O_2,mitochondrial membrane potential in HSPB1 and control H9c2 cells were (10.0?0.11)vs (7.01?0.26),(9.11?0.17)vs (6.05?0.19),(7.69?0.28)vs (5.14?0.28),(6.95?0.13)vs (4.66?0.11),(6.61?0.20)vs (1.85?0.35),(6.60?0.05)vs (1.19?0.01),respectively (all P0.05).Conclusions HSPB1 protects rat cardiomyocytes cell line(H9c2) from oxidative damage,which suggests that stabilization of mitochondrial membrane potential and the decreased endogenous reactive oxygen species after oxidative stress may be involved in the protection of HSPB1 against oxidative stress in H9c2.