Molecular docking technology and network pharmacology based on Rhapontici Radix-Cremastrae Pseudobulbus drug pair in treating breast cancer.

OBJECTIVE: Network pharmacology is a bioinformatics-based research strategy for identifying the mechanisms of drugs and promoting drug development. This study used network pharmacology to investigate the mechanism of the Loulu-Cremastrae Pseudobulbus drug pair treating breast cancer (BC). MATERIALS AND METHODS: The ingredients and potential targets of the drug pair were searched with Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCSMP). National Center for Biotechnology Information (NCBI) and gene cards were used to search the targets of BC. Networks of "drugs-components-targets" and protein-protein interaction were constructed through Cytoscape. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were carried out through common targets. Using AutoDock tool, molecular docking was performed to verify the binding between key targets and compounds. RESULTS: Finally, we selected 6 active compounds from the drug pair. A total of 61 targets were associated with the drug pair, and 15,295 targets were related to BC. 55 common targets were obtained after the intersection. The key targets included Transcription factor Jun (JUN), Heat shock protein HSP 90-alpha (HSP90AA1), and Caspase-3(CASP3). 327 terms were obtained by GO analysis. 78 pathways (p < 0.05) were identified through KEGG analysis. Molecular docking indicated that important compounds combined well with key targets. CONCLUSIONS: Various active compounds, including beta-sitosterol, 2-methoxy-9,10-dihydrophenanthrene-4,5-diol, and stigmasterol, can regulate multiple signaling pathways related to BC, such as the estrogen and prolactin signaling pathways, playing therapeutic roles in BC.

[Textual research on the birthplace of Chen Xunzhai, a doctor of the Republic of China].

Chen Xunzhai was a famous Fujian traditional Chinese medicine expert in the period of the Republic of China. There are different records of his native place in the existing literature. By reviewing the published journals and books, interviewing Chen Xunzhai's scattered works and genealogy and visiting his descendants, this article conducted investigations and researches and confirmed that Chen Xunzhai, also named Guangcheng, was born in Shangyang Village, Gaopo Town in Yongding County of Fujian Province. He was the 22nd generation of descendants of Chen family in Shangyang Yingchuan County, not the descendant of the Chen family in Jiang Tian Nanyang of Chang Le City. Neither was he the seventh-generation grandson of Chen Xiuyuan. The findings of this paper will lay the foundation for the further researches on Chen Xunzhai.

[The library of Chinese Medical Association in the Republican Period].

The library of Chinese Medical Association was founded in 1925. The source of books and periodicals in the library are mainly from purchasing and donation. The library provides services such as lending, exchanging books, translating and publishing the contents and abstracts of medical journals in Chinese and other languages. It has played an active and important role in promoting medical development in the period of Republic of China.

[The study of using salvianolate treat acute lung injury in rats induced by paraquat].

Objective: To establish to paraquat poisoning acute lung injury animal model to study the therapeutic effect of Salvia polyphenols acid salt of paraquat-induced acute lung injury. Methods: Adult male Wister rats 120, were randomly divided into three groups: the paraquat exposure group, the start of the experiment to give a one-time 20% paraquat dope orally 50 mg/kg body weight of rats; salvianolate treatment group, the start of the experiment paraquat to give a one-time 20% the stock solution orally 50 mg/kg body weight of rats, and then given daily intraperitoneal injection of 200 mg/kg body weight of rats salvianolate; blank control group was given the same amount normal saline. The exposure group, the treatment group and control group rats were sacrificed after anesthesia in the 3rd, 7th, 14th, 21st day from the beginning of the experiment respectively, and taken out and preserved venous blood specimens and lung tissue to be tested. Venous detection heme oxygenase-1 (HO-1) , the lung tissue detection heme oxygenase-1 (HO-1) , hydroxyproline (HYP) . And do biopsy specimens from some of the lung tissue, HE and Masson staining observed by optical microscope. Results: Compared with control group, model group 7, 14, 21 days had elevated levels of serum and lung tissue HO-1 (all P<0.05) ; Treatment group 3, 7, 14, 21 days increased (all P<0.05) , and 3, 7, 14 days is higher than the model group (compared with model group, P<0.05) . Compared with control group, treatment group 3 days and model group, 14, 21 days HYP content in lung tissue increased significantly (all P<0.05) ; 21 days, compared with model group, HYP content of treatment group reduce obviously, the difference was statistically significant (P<0.05) . Optical microscope observation, lung tissue damage and aggravated with the experimental increase in the number of days, inflammatory cell infiltration, alveolar septal fibrosis gradually formed. The treatment group experimental animal lung tissue to reduce inflammation, lung fibrosis relief. Conclusion: Paraquat (50 mg/kg body weight) to fill the stomach can be induced model of acute lung injury in the rats. The serum HO-1 expression and HO-1, HYP content in lung tissue increased obviously in model rats. Salvia miltiorrhiza polyphenols acid salt to a certain degree and stage influenced the expression of HO-1 and HYP, relieve acute lung injury and pulmonary fibrosis, has certain curative effect in the treatment of paraquat poisoning.

Phosphoinositide 3-kinase inhibitor LY294002 ameliorates the severity of myosin-induced myocarditis in mice.

BACKGROUND: Myocarditis, characterized by myocyte necrosis, fibrosis, and degeneration with mononuclear cell infiltration, always causes heart failure in patients. Phosphoinositide 3-kinase (PI3K) is a pivotal kinase known to regulate inflammatory responses in cardiac diseases. Although previous research has suggested that PI3K was involved in cardiac diseases such as myocardial infarction, it is still unclear whether the inhibition of PI3K is essential for the treatment of myosin-induced myocarditis. The aim of this study was to explore whether pharmacological blockade of PI3K is able to protect mice against experimental autoimmune myocarditis (EAM). MATERIALS AND METHODS: We used the cardiac myosin-induced murine EAM model to investigate the therapeutic effect of PI3K inhibitor LY294002 on autoimmune myocarditis in mice. RESULTS: LY294002 significantly alleviated EAM injury in mice, as indicated by the reduction of cardiac necrosis, inflammatory infiltrates, and CD3(+) T cells. LY294002 also decreased the expression of p-Akt upon cardiac myosin treatment in the cardiac tissue of the mice. In the present study, LY294002 resulted in a moderate reduction in absolute CD4(+) cell numbers and a significant decrease in the absolute numbers of CD8(+) cells. Consequently, LY294002 increased the CD4(+)/CD8(+) ratio compared with peptide treatment alone. CONCLUSION: This report provides evidence that PI3K inhibitor LY294002 has potent effects against cardiac injury caused by EAM, suggesting that it has therapeutic value for the treatment of myocarditis.

[Ten-day Periodical of Traditional Chinese Medicine and its concept of confluence of Chinese and western medicine].

The Ten-day Periodical of Traditional Chinese Medicine, a TCM Journal founded by the Xiamen Professional School of Traditional Chinese Medicine in July 1934, had published a lot of essays written by many TCM physicians that interpret the concept of traditional Chinese medicine by western medicine, offering the academic way of probing confluence of Chinese and Western Medicine in Xiamen. The aim of the Journal includes "developing TCM academy" and the "confluence of TCM with western medicine" , the exploration of TCM and the penetration of Chinese and western medicine, and getting rid of blind faith on "science" to set up the belief of TCM and to prove the ideas of visceral theory and its gasification by the anatomical knowledge of western medicine. The Journal envisaged the difference between the TCM and WM, avoided blind convergence, representing the academic inheritance and progress of the era. Although the essays published might have made a forced analogy by over-praising TCM, however, its exploration and convergence of TCM and the experiences are helpful to modern scholars to properly manage the relation of TCM and WM to face the future challenge consciously.

In vivo toxicity of nano-alumina on mice neurobehavioral profiles and the potential mechanisms.

The rapid development and expanding applications of nanotechnology have led to enhanced exposure of human body to nanoparticles. It is, therefore, necessary to address the safety issue via rigorous toxicological evaluation and to understand the underlying interaction mechanism. However, only a few studies to date have evaluated the safety of nano-sized materials and their potential adverse effects on biological systems. In this study, we sought to investigate the potential toxicity of aluminum oxide (alumina) nanoparticles in ICR strained mice, focusing on potential neurobehavioral defects and the possible mechanisms. The results demonstrated that nano-alumina impaired neurobehavioral functions, including lengthened escape latency, shorter time spent in the target quadrant and reductions in the number of platform crossing. In addition, it induced cell necrosis and apoptosis, which were likely mediated by the reduction of MMP and ROS, and the induction of the caspase-3 gene. Our results implicated that mitochondrial impairment plays a key role in neurotoxicity of nano-alumina, sequent oxidative damage and neural cell loss, especially necrosis, may be direct causes for the neurobehavioral defects. Collectively, nano-alumina presents a strong pro-cell death effect on ICR mice in vivo, suggesting that nano-alumina may serve as an inducer for neural toxicology. Findings in the present study indicating that surface chemical characteristics and nanoscale sizes of nano-alumina could co-contribute significantly to neurotoxicity. The impaired neurobehavioral patterns indicate that nano-alumina particles are more toxic to the cerebrum than those of nano-carbon with the same nanoparticle size and micro-alumina with the same surface chemical characteristics.

The role of leptin resistance in the lipid abnormalities of aging.

Leptin resistance has been implicated in the pathogenesis of obesity-related complications involving abnormalities of lipid metabolism that resemble those of old age. To determine whether development of leptin resistance in advancing age might account for such abnormalities, we compared the effects of hyperleptinemia (>40 ng/ml) induced in 2-month-old and 18-month-old lean wild-type (+/+) Zucker diabetic fatty rats by adenovirus gene transfer. The decline in food intake, body weight, and body fat in old rats was only 25%, 50%, and 16%, respectively, of the young rats. Whereas in young rats plasma free fatty acids fell 44% and triacylglycerol (TG) 94%, neither changed in the rats. In hyperleptinemic young rats, adipocyte expression of preadipocyte factor 1 increased dramatically and leptin mRNA virtually disappeared; there was increased expression of acyl CoA oxidase, carnitine palmitoyl transferase 1, and their transcription factor peroxisome proliferator-activated receptor alpha, accounting for the reduction in body fat. These hyperleptinemia-induced changes were profoundly reduced in the old rats. On a high-fat diet, old rats consumed 28% more calories than the young and gained 1.5x as much fat, despite greater endogenous hyperleptinemia. Expression of a candidate leptin resistance factor, suppressor of cytokine signaling 3 (SOCS-3), was compared in the hypothalamus and white adipocytes of young and old rats before and after induction of hyperleptinemia; hypothalamic SOCS-3 mRNA was approximately 3x higher in old rats before, whereas it was 3x higher in WAT after, hyperleptinemia. We conclude that the anorexic and antilipopenic actions of leptin decline with age, possibly through increased SOCS-3 expression, and that this could account for the associated abnormalities in lipid metabolism of the elderly.

Liporegulation in diet-induced obesity. The antisteatotic role of hyperleptinemia.

To test the hypothesis that the physiologic liporegulatory role of hyperleptinemia is to prevent steatosis during caloric excess, we induced obesity by feeding normal Harlan Sprague-Dawley rats a 60% fat diet. Hyperleptinemia began within 24 h and increased progressively to 26 ng/ml after 10 weeks, correlating with an approximately 150-fold increase in body fat (r = 0.91, p < 0.0001). During this time, the triacylglycerol (TG) content of nonadipose tissues rose only 1-2.7-fold implying antisteatotic activity. In rodents without leptin action (fa/fa rats and ob/ob and db/db mice) receiving a 6% fat diet, nonadipose tissue TG was 4-100 times normal. In normal rats on a 60% fat diet, peroxisome proliferator-activated receptor alpha protein and liver-carnitine palmitoyltransferase-1 (l-CPT-1) mRNA increased in liver. In their pancreatic islets, fatty-acid oxidation increased 30% without detectable increase in the expression of peroxisome proliferator-activated receptor-alpha or oxidative enzymes, whereas lipogenesis from [14C]glucose was slightly below that of the 4% fat-fed rats (p < 0.05). Tissue-specific overexpression of wild-type leptin receptors in the livers of fa/fa rats, in which marked steatosis is uniformly present, reduced TG accumulation in liver but nowhere else. We conclude that a physiologic role of the hyperleptinemia of caloric excess is to protect nonadipocytes from steatosis and lipotoxicity by preventing the up-regulation of lipogenesis and increasing fatty-acid oxidation.

Comparing the hypothalamic and extrahypothalamic actions of endogenous hyperleptinemia.

To determine whether the depletion of body fat caused by adenovirus-induced hyperleptinemia is mediated via the hypothalamus, we used as a "bioassay" for hypothalamic leptin activity the hypothalamic expression of a leptin-regulated peptide, cocaine- and amphetamine-regulated transcript (CART). The validation of this strategy was supported by the demonstration that CART mRNA was profoundly reduced in obese rats with impaired leptin action, whether because of ablation of the ventromedial hypothalamus (VMH) or a loss-of-function mutation in the leptin receptor, as in Zucker diabetic fatty rats. We compared leptin activity in normal rats made hyperleptinemic by adenovirus-leptin treatment (43 +/- 9 ng/ml, cerebrospinal fluid leptin 100 pg/ml) with normal rats made hyperleptinemic by a 60% fat intake (19 +/- 4 ng/ml, cerebrospinal fluid leptin 69 +/- 22 pg/ml). CART was increased 5-fold in the former and 2-fold in the latter, yet in adenovirus-induced hyperleptinemia, body fat had disappeared, whereas in high-fat-fed rats, body fat was abundant. Treatment of the high-fat-fed rats with adenovirus-leptin further increased their hyperleptinemia to 56 +/- 6 ng/ml without changing CART mRNA or food intake, indicating that leptin action on hypothalamus had not been increased. Nevertheless, their body fat declined 36%, suggesting that an extrahypothalamic mechanism was responsible. We conclude that in diet-induced obesity body-fat depletion by leptin requires supraphysiologic plasma concentrations that exceed the leptin-transport capacity across the blood-brain barrier.

[Observation of therapeutic effect by combined administration of Salvia miltiorrhiza, ligustrazine and Panax notoginseng on late hemorrhagic shock of rabbits].

OBJECTIVE: To explore the therapeutic mechanism of Salvia miltiorrhize, ligustrazine and Panax notoginseng in treating late hemorrhagic shock in rabbit. METHODS: Rabbit hemorrhagic shock models (MPA 5.3 kPa) were set up according to Wiggers' method and administrated Salvia miltiorrhiza, ligustrazine, Panax notoginseng. The values of blood RBC superoxide dismutase (SOD) and blood lactate (BL), plasma malondialdehyde (MDA) and magnesium (Mg++) were continuously monitored before shock, 120 minutes after shock, 60 and 120 minutes after hydraulic dilatation. RESULTS: (1) In 120 minutes after shock, the level of SOD decreased and the concentrations of MDA, BL, Mg++ were markedly increased, which indicated that the cell membrane damage caused by oxygen free radicals in rabbit hemorrhagic shock. (2) Salvia miltiorrhiza, Ligustrazine or Panax notoginseng could alleviate lipidperoxidation injury to tissue. Compared with the single drug administration groups, the effects of oxygen free radicals scavangers by combined administration with half dose of 2 drugs were better than the single drug with full dose alone and the side effects such as depression of blood pressure and heart rates would be alleviated. CONCLUSION: Combined administration of Salvia miltiorrhiza, ligustrazine and Panax notoginseng would half the dosage, the blood pressure depression and heart rate reduction alleviated and better result obtained.