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Diabetic cardiomyopathy, one of the cardiovascular complications of diabetes, is characterized by cardiac systolic and diastolic dysfunction at the early stage, which can later develop into heart failure. Due to the high incidence and mortality, it has been a hot topic in recent years. The pathogenesis of diabetic cardiomyopathy is complicated. It has been proved related to abnormal glucose and lipid metabolism, cardiac insulin resistance, mitochondrial dysfunction, abnormal calcium homeostasis, activation of renin-angiotensin-aldosterone system, increased oxidative stress, endoplasmic reticulum stress, inflammation, autophagy, and so on. The specific pathogenesis remains unclear. Currently, the diabetic cardiomyopathy is mainly tackled with both western medicine and traditional Chinese medicine (TCM). Traditional western medicine has no specific remedy for diabetic cardiomyopathy, and the resulting side effect cannot be neglected. In order to improve the efficacy and reduce the side effects, researchers have tried some potential medical treatments, such as vaspin, melatonin, Coenzyme Q10, and non-coding RNA, which still need further clinical trials. Diabetic cardiomyopathy is not recorded in ancient TCM books. According to the symptoms and signs, modern physicians often consider it as a "consumptive disease", whose main therapeutic principles lie in benefiting Qi, tonifying Yin, activating blood, and removing stasis. The individual Chinese herbs such as Astragali Radix and Salviae Miltiorrhizae Radix et Rhizoma and Chinese herbal compounds like Huotan Jiedu Tongluoyin are effective in protecting the heart. But there are few studies exploring the pharmacodynamic mechanisms of TCM. With the continuous emergence of new drugs, the integration of TCM with western medicine may be a more promising treatment in the future. In conclusion, the pathogenesis of diabetic cardiomyopathy is unclear, and there is a lack of effective prevention and treatment. This paper reviewed the latest findings in pathogenesis and treatment of diabetic cardiomyopathy, in order to provide reference for further research.
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Diabetic retinopathy (DR) is one of the microvascular complications of diabetes. At present, the pathogenesis of DR is obscure and drugs can not meet clinical needs, however. Experimental animal model of DR is an effective tool to study its pathogenic mechanism and evaluate drug efficacy. In this paper, the research progress of experimental animal models of DR has been-reviewed in recent years, mainly using mice, zebrafish, and other experimental animals, which can be divided into two categories: induced type and genotype, according to the inducer.
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Scutellarin is a flavonoid extracted from breviscapus, a traditional Chinese medicine. Pharmacological studies have shown that scutellarin has anti-inflammatory, antioxidant, anti-fibrosis, anti-tumor, improving cardiac and cerebral ischemia. In recent years, with the deepening of research on scutellarin, it was found that it could inhibit the tumor through multi-target and multi-pathway, and the anti-human colorectal cancer was related to the regulation of p53 pathway, Hedgelog pathway and erythropoietin generates liver cancer interactivator B2(EphrinB2).The anti-esophageal squamous cell carcinoma is related to protein kinaseB1 /protein kinaseB2( Akt1/Akt2).Anti-renal carcinoma and melanoma are associated with phosphatase and tension protein homologues(PTEN) and phosphatidylinositol 3-kinase(PI3K)/Akt/mammalian target of rapamycin(mTOR) pathway. Anti-lung cancer is related to Akt/mTOR/4E binding protein1(4EBP1) and signal transduction and transcriptional activator(STAT3 )signaling pathway. Anti-cervical cancer is related to pyruvate kinase 2(PKM2).Anti-breast cancer is associated with Hippo/YAP pathway. At the same time, scutellarin was found to prevent diabetic microangiopathy, atherosclerosis and non-alcoholic fatty liver disease by regulating glucose and lipid metabolism, but the mechanism of action was not well studied. A review of the literature found that scutellarin anti-tumor, atherosclerosis, diabetic microangiopathy, non-alcoholic fatty liver disease, osteoarthritis, osteoporosis mechanism of action lack of detailed summary. In this paper, the research progress of pharmacological action and mechanism of scutellarin in recent 5 years is reviewed, and Suggestions on its current research status and future direction are put forward, in order to speed up the discovery of pharmacological mechanism of scutellarin and provide scientific basis for its further development and utilization.
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Objective::To investigate the protective effect of salvianolic acid B on HepaRG hepatocyte injury induced by arsenic trioxide (As2O3 ) and its mechanism. Method::HepaRG cells were incubated with 5μmol·L-1 As2O3 for 24 h to induce hepatocyte injury. The cells were divided into control group, model group, salvianolic acid B 10 μmol·L-1 group, salvianolic acid B 10 μmol·L-1+ As2O3 group, salvianolic acid B 5 μmol·L-1+ As2O3 group, and salvianolic acid B 2.5 μmol·L-1+ As2O3 group. HepaRG cells were preincubated with salvianolic acid B for 2 h and then incubated with As2O3 for 24 h. At the end of the incubation, cell viability was detected by thiazolyl blue tetrazolium bromide assay, apoptosis was observed by Hoechst33342 fluorescence staining, apoptosis rate was detected by annexin V-FITC/propidium iodide double staining flow cytometry, and mitochondrial membrane was observed by JC-1 fluorescence staining. Western blot was used to detect the protective effect of expressions of relevant proteins Bcl-2, Bax, Akt, p-Akt on salvianolic acid B in the liver. Result::As2O3 concentration-dependently reduced the survival rate of HepaRG cells(P<0.01), salvianolic acid B had no effect on normal cell viability for 2 h, pre-incubation with salvianolic acid B(5, 10 μmol·L-1) for 2 h significantly increased the decreased cell survival rate caused by As2O3 (P<0.01). As2O3 significantly increased hepatocytes apoptosis rate(P<0.01), while pre-incubation with salvianolic acid B(10 μmol·L-1) deceased apoptosis rate(P<0.01). Incubation with As2O3 for 24 h caused decrease of mitochondrial membrane potential, pre-incubation with salvianolic acid B maintained mitochondrial membrane potential, indicating that the anti-apoptotic effect of salvianolic acid B were related to the mitochondrial pathway modulation. Western blot analysis showed that salvianolic acid B promoted the ratio of Bcl-2/Bax and promoted p-Akt/Akt compared with As2O3 group(P<0.01). Conclusion::Salvianolic acid B has a protective effect on hepatocyte injury induced by As2O3, and its mechanism is related to maintenance of mitochondrial function and inhibition of hepatocyte apoptosis.
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Erigeron breviscapus, a species within the genus of Erigeron, is mainly distributed in Southwest China. It is cold in property, slightly bitter in taste, and has the effect of dispersing cold table, removing wind and dehumidification, promoting blood circulation and removing blood stasis, relieving pain and inflammation. Breviscapine is the extract of E. breviscapus. It is mainly consisted of flavonoids, lignans, coumarins, terpenes, phytosterols, etc. As the major components of breviscapine, the content of breviscapine b (4′-hydroxybaicalin-7-O-glucuronide) and breviscapine a (apigenin-7-O-glucuronide) is greater than 90%. Modern pharmacological studies have shown that breviscapine has a wide range of pharmacological effects, including anti-oxidation, anti-fibrosis, anti-inflammation, anti-aging, anti-platelet aggregation, lowering blood lipid, increasing blood flow, improving microcirculation, preventing and treating tumors, and resisting brain injury. In clinical, breviscapine has been widely used in the treatment of diabetes, cerebral insufficiency, sequelae caused by cerebral hemorrhage, hypermucolipemia, cerebral thrombosis, kidney disease, liver disease, Alzheimer's disease, and some other complex diseases. Specially, in the treatment of diabetes and its chronic complications, such as diabetic nephropathy, diabetic cardiomyopathy, diabetic foot, diabetic retinopathy, breviscapine has showed significant efficacy. In addition, studies have demonstrated that the combined application of breviscapine, mecobalamine, and micopol can improve the therapeutic effect. In this work, the application of breviscapine in the treatment of chronic complications of diabetes mellitus and its related combination drugs were reviewed, by which we attempted to provide some valuable clues for the clinical application of breviscapine in the treatment of diabetes mellitus and its chronic complications.
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<b>Objective::To study the protective effect and mechanism of Qidong Yixin oral liquid on doxorubicin-induced myocardial toxicity in mice. <b>Method::Ninety male ICR mice were randomly divided into normal group, model(DOX) group, DOX+ Qidong Yixin oral liquid group (9.55, 23.88, 47.75 g·kg<sup>-1</sup>) and high dose group (47.75 g·kg<sup>-1</sup>) with 15 mice in each group. The normal group and model group were given pure water by gavage, and each dose group of Qidong Yixin oral liquid was given different doses of Qidong Yixin oral liquid once a day for 21 days. On the seventh day, normal saline was injected into the abdominal cavity of the normal group and the high dose group of Qidong Yixin oral liquid. Doxorubicin was injected into the abdominal cavity of the other groups (15 mg·kg<sup>-1</sup>). After 21 days, the weight and heart weight of mice were weighed and cardiac index was calculated. Serum was taken for the detection of lactate dehydrogenase (LDH), creatine kinase (CK), aspartate aminotransferase (AST). Heart was taken for hematoxylin-eosin (HE) staining, superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), catalase (CAT) in myocardial tissue were detected. The expression of nuclear factor NF-E2 related factor (Nrf2) and heme oxygenase-1 (HO-1) were detected by Western blot. <b>Result::Compared with normal group, adriamycin could significantly reduce the body weight of mice (<italic>P</italic><0.01), increase the activities of LDH, CK and AST in serum(<italic>P</italic><0.01), and decrease the activities of antioxidant enzymes (<italic>P</italic><0.01). Compared with DOX group, high dose Qidong Yixin oral liquid could significantly increase the weight of mice (<italic>P</italic><0.05, <italic>P</italic><0.01), decrease the level of myocardial three enzymes(<italic>P</italic><0.01), increase the activity of antioxidant enzymes(<italic>P</italic><0.05, <italic>P</italic><0.01), and increase the expression of Nrf2 and HO-1(<italic>P</italic><0.01). <b>Conclusion::Qidong Yixin oral liquid has a good protective effect on doxorubicin myocardial toxicity. Its mechanism may be related to activating Nrf2/HO-1 signaling pathway and alleviating oxidative stress injury.
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Diabetic kidney disease(DKD) has become a primary cause of end-stage kidney disease, without any effective treatment available. In this study, we assessed the protective effect of Guanxin Danshen Formulation(GXDSF) on diabetic nephropathy in db/db mice. The db/m and db/db mice were randomly divided into 4 groups: control group, model group, metformin group, and GXDSF group. After 8 weeks' treatment with GXDSF, metformin or normal saline, the mice were sacrificed, and the blood and kidney tissues were collected for the further analysis. Compared with the model group, TG, TCH and LDL levels significantly decreased in the GXDSF group. The results from HE and PAS staining showed that db/db mice exhibited abnormal kidney tissues with increased glomerular volume, basement-membrane thickening and mesangial cell proliferation, which could be significantly alleviated by GXDSF treatment. GXDSF treatment also reduced serum creatinine and BUN. Meanwhile, GXDSF treatment markedly elevated GSH-PX levels, while reduced LDH and MDA levels in the kidney tissues. Western blot assay showed that GXDSF evidently up-regulated protein levels of ERα and p-Akt, and subsequently promoted HO-1 expression mediated by Nrf2. These data collectively indicated that GXDSF protects db/db mice against DN by regulating ERα and Nrf2-mediated HO-1 expression.
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Animais , Camundongos , Creatinina , Diabetes Mellitus , Nefropatias Diabéticas , Rim , Glomérulos Renais , Fator 2 Relacionado a NF-E2 , Salvia miltiorrhizaRESUMO
The aim of this paper was to investigate the preventive effects of Keluoxin Capsules(KLX) on diabetic retinopathy in db/db mice. One hundred male db/db diabetic mice(45-55 g, 8 weeks) were randomly divided into 5 groups(model, KLX low dose, KLX middle dose, KLX high dose, Dobesilate) and 20 male C57 BL/KsJdb~(+/+) were taken as control group. Body weight and fasting blood-glucose were detected every week. Mice were administrated with saline(control and model group), KLX(780, 1 560, 3 120 mg·kg~(-1)·d~(-1), ig), Dobesilate(195 mg·kg~(-1)·d~(-1), ig) for 20 weeks, respectively. At the end of the administration, optical coherence tomography, fundus fluorescein angiography and electroretinogram of the retina were measured. The eyeball was extirpated and retina was isolated to make paraffin section, followed by HE staining and glial fibrillary acidic protein(GFAP) immunohistochemistry. The results indicated that KLX has no obvious effect on body weight and fasting blood level in db/db mice. However, KLX could significantly regulate the thickness of retinal ganglion layer and inner plexiform layer. KLX was able to remarkably reduce the quantity of diabetic microvessel. Meanwhile, KLX could notably improve retinal function. Moreover, KLX could observably modulate the cell arrangement and edema in each layer. There was no markable difference in retina according to the immunochemistry assay. In the present study, KLX exert marked preventive effects on diabetic retinopathy in db/db mice, which provided an experimental evidence for clinical use.
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Animais , Masculino , Camundongos , Cápsulas , Diabetes Mellitus Experimental , Retinopatia Diabética , Tratamento Farmacológico , Angiofluoresceinografia , Hipoglicemiantes , Farmacologia , Distribuição Aleatória , RetinaRESUMO
To investigate the effect of scutellarin (Scu) on diabetic cardiomyopathy in mice, type 2 diabetes mellitus was induced by intraperitoneal injection of 50 mg∙kg-1 streptozotocin (STZ) into a high-fat diet. Scu was injected intraperitoneally. After 8 weeks, fasting blood glucose and serum biochemical parameters were measured. Masson staining was performed on myocardial tissue. The expression levels of Nrf2, NFκB, AKT and p-AKT in myocardium of mice were observed by Western blot. All the procedures were approved by the Laboratory Animal Ethics Committee of the Peking Union Medical College. The results showed that Scu significantly decreased the heart-body ratio, increased myocardial contractile function, decreased the level of myocardial fibrosis and the expression of collagen I and collagen III in myocardium of diabetic mice. Scu can effectively reduce the levels of lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB), malondialdehyde (MDA) in serum of diabetic mice, increase the level of antioxidant enzymes in serum, and inhibit the release of inflammatory factors. Further studies showed that Scu significantly increased Nrf2 nuclear translocation, inhibited NFκB nuclear translocation and increased AKT phosphorylation. It indicates that Scu has significant effect on diabetic cardiomyopathy in mice.
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Diabetic cognitive dysfunction (DCD) is a common chronic complication of diabetes mellitus with sophisticated path-ogenesis which has not yet been fully elucidated. In this review paper, the mechanisms of metabolic abnormalities, insulin re-sistance,endoplasmic reticulum stress,neuronal calcium dysho-meostasis, in ammation, blood brain barrier impairment, and mitochondrial injury associated with DCD are reviewed. In addi-tion,the prevention and treatment of DCD by traditional Chinese medicines (TCMs) and the effective compounds are comprehen-sively summarized, in order to provide an updated overview on the DCD pathogenesis,as well as the scientific evidence under-pinning the use of TCM interventions for the treatment and pre-vention of DCD.
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Aim To probe into the bavachinin toxic mechanisms in HepaRG cells. Methods MTT assay was used to determine toxicity and dose. After treated with 6.25,12.5 and 25 μmol·L-1bavachinin for 24 h,the cell death was investigated by Hoechst 33342/PI,LDH,caspase-3 activity,and Bax,Bcl-2 expression levels. Mitochondrial damage was detected by mito-chondrial membrane potential,ATP content,openness of mitochondrial permeability transition pore and cyto-chrome C level. Results Bavachinin administration up-regulated Bax/Bcl-2 ratio and caspase-3 activity with increase of drug concentration after 24 h. Apop-totic rate increased in a dose-dependent manner be-tween 6.25 and 25 μmol·L-1,but when reached to 25 μmol·L-1,cells showed more necrosis. Mitochon-drial injury indicators significantly increased after 24h. Conclusion Bavachinin induces HepaRG cell apopto-sis and necrosis through mitochondria injury.
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Atherosclerosis, as a chronic inflammatory disease, is the most common one among cardiovascular system disorders. Inflammation is crucial in the development of atherosclerosis, which participates in the entire process of atherosclerosis. NF-κB can target to most inflammatory factors, and excessive NF-κB activation aggravates atherosclerosis development. Previous stud- ies have shown that the zinc finger protein A20 plays a key role in the anti-inflammatory and anti-apoptotic response. Research advances on A20 in protection of atherosclerosis are thus summa-rized in this review.
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It is now thought that atherosclerosis,although due to enhanced lipid deposition,is mainly the result of a series inflammatory process.Total saponins of Aralia elata (Miq)Seem(TASAES)from the Chinese traditional herb Longya Araliachinensis L.,a folk medicine used for treating various diseases, increasing energy and improving the body′s ability to prevent hypoxia in Asian countries has attracted widespread attention. However, the ability of TASAES on inflammation-triggered vascular endothelial cell injury, a key early event in the pathogenesis of atherosclerosis, and its potential mechanisms of this protection have never been demonstrated. The present study determined the anti-inflammatory and anti-apoptoticactivities and protective mechanisms of the total aralosides of Araliaelata(Miq)Seem (TASAES) ameliorate tumor necrosis factor-α (TNF-α)-induced human umbilical vein endothelial cells (HUVECs) injury. Our results indicate that TASAES pretreatment provided cytoprotective effects by suppressing TNF-α-induced HUVECs apoptosis, mitochondrial membrane depolarization, caspase-3 activation, and modulation of inflammatory factors (IL-6, MCP-1 and VCAM-1), meanwhile inhibiting NF- κB transcription. Furthermore, the effect was correlated with the activation of the PI3K/Akt signal pathway. Blocking Akt activation with the PI3K inhibitor LY294002 effectively reversed the protective effect of TASAES against TNF-α-induced cell apoptosis.Moreover,the PI3K inhibitor partially blocked the effects of TASAES on the increasing of Bcl-2 and Bcl-xl protein expression,and inactivation of Bax protein expression. In conclusion, the results showed that TASAES decreased the inflammation and apoptosis of HUVECs caused by TNF-α treatment,and PI3K played a crucial role in enhancing cell sur-vival during this process.
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By retrieving domestic and foreign literatures, the authors provided a systematic review for effects of Xanthii Fructus, toxicity recorded in ancient/current literatures and relevant toxicological experience, and summarized clinical characteristics of clinical cases related to Xanthii Fructus and influencing factors. In addition to liver and kidney injuries as the major side effects of Xanthii Fructus, neurotoxicity and cardio-toxicity of Xanthii Fructus were also common clinical adverse events. However, there have been a few animal experimental studies so far. Oral administration and external application with Xanthii Fructus have often caused skin reactions, even such severe cases as exfoliative dermatitis. The authors suggested standardizing the clinical medication, avoiding to use untreated prescriptions and unprocessed herbs, ensuring the effective and safety use of Xanthii Fructus in strict accordance with the recommended dosage and usage in pharmacopeia, paying attention to the accumulation of safety signals, strengthening studies on toxic substance, toxicity mechanism, and synergy and attenuation effects.
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The authors systemically evaluated and analyzed the safety of Areca catechu from domestic and foreign literatures about the herbal origin, toxicity recorded in ancient/current documents, safety case reports of clinical A. catechu, experimental studies on toxicity in recent years, and differences of safety risk between edible and medicinal A. catechu. Subsequently, they proposed a preliminary summary about the clinical characteristics and potential risk factors of safety related cases of A. catechu and its preparations. According to the authors, although clinical adverse events of A. catechu were fewer and controllable, clinicians shall stillstrictly standardize its application, and rationally combine it with other herbs, while strengthening fundamental and clinical studies related to safety, so as to give better guidance to safety application of A. catechu in clinic.
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Through a systematic and comprehensive study of domestic and foreign literatures and information, this study aims to trace the herbal origin and the toxicity recorded in ancient and current documents, analyze the safety case reports of Psoralea corylifolia and experimental studies on toxicity in recent years, and make a preliminary summary about the clinical characteristics and potential risk factors of cases related to the safety of P. corylifolia and its preparations. The study involved 84 patients in the safety case reports of P. corylifolia. The adverse events were mainly liver damage (55.95%) and light toxic contact dermatitis (38.10%), sugguesting that P. corylifolia may lead to liver damage and photo toxicity. However, reproductive toxicity and renal damage were only reported in animal studies, but not in clinical reports. Because of its complicated ingredients, the toxic components and mechanisms of P. corylifolia have not been clear at present. Therefore, the authors proposed to strictly apply P. corylifolia in clinic, use it rationally and combine it with other medications. Besides, efforts shall be made to strength the guidance for doctors, the safety monitoring of P. corylifolia and relevant preparations, and actively carry out safety-related basic and clinical studies, so as to give a better guidance to safe medication, full exert the efficacy and avoid the medication risk.
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Twenty-eight compounds were isolated and purified from Clinopodium chinense by Sephedax LH-20, ODS, MCI and preparative HPLC. Their structures were identified as apigenin (1), apigenin-7-O-β-D-glucopyranoside (2), apigenin-7-O-β-D-glucuronopyranoside (3), thellungianol (4), apigenin-7-O-β-D-rutinoside (5), luteolin (6), luteolin-4'-O-β-D-glucopyranoside (7), apigenin-7-O-β-D-pyranglycuronate butyl ester (8), luteolin-7-O-β-D-rutinoside (9), luteolin-7-O-β-D-noehesperidoside (10), acacetin (11), acacetin-7-O-β-D-glucuronopyranoside (12), buddleoside (13), naringenin (14), pruning (15), nairutin (16), isosakuranetin (17), isosakuranin (18), didymin (19), hesperidin (20), kaempferol (21), quercetin (22), kaempferol-3-O-α-L-rahmnoside (23), p-hydroxycinnamic acid (24), caffeic acid (25), cis-3-[2-[1-(3,4-dihydroxy-phenyl)-1 -hydroxymethyl]-1,3-ben-zodioxol-5-yl]-(E)-2-propenoic acid (26), mesaconic acid (27), gentisic acid 5-O-β-D-(6'-salicylyl)-glucopyranoside (28). Among them, compounds 7, 9-10, 12, 23, 26-28 were isolated from the Clinopodium for the first time. The protective effects of compounds 1-6, 8-17 and 19 against H2O2-induced H9c2 cardiomyocyte injury were tested, compounds 15 exhibited significantly protective effects. Compared with the cell viability of (62.12±6.18)% in the model, pruning exhibited viabilities of (84.25±7.36)% at 25.0 mg•L⁻¹, respectively, using quercetin as a positive control [cell viability of (84.55±8.26)%, 20 mg•L⁻¹].
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To observe the hypoglycemic effect of Qizhi Jiangtang capsule in rats with type 2 diabetes, and investigate the preliminary mechanism of its hypoglycemic effect, type 2 diabetes rat models were established by high glucose and high fat combined with small dose of streptozotocin (STZ). After continuous administration for 6 weeks, blood glucose, and glycosylated serum protein (GSP) levels were detected in all of the animals; immunohistochemistry assay was used to detect the number of islet β cells; Western blot assay was used to detect the protein expression levels of insulin receptor (InsR), phosphoinositide-3 kinases (PI3K), glucose transporter-2 (GLUT2) and phosphorylated Jun N-terminal kinases (p-JNK)in hepatic tissues. The results showed that Qizhi Jiangtang capsule could reduce the blood sugar and GSP levels in serum in animals with type 2 diabetes mellitus, increase the level of insulin in serum and number of islet β cells, increase the protein expression levels of InsR, PI3K and GLUT2, and reduce the level of p-JNK protein expression. In conclusion, Qizhi Jiangtang capsule has relatively stable hypoglycemic effect, and the mechanism may be associated with increasing the number of islet β cells and level of insulin in serum, up-regulating the protein expression levels of InsR, PI3K and GLUT2, down-regulating the level of p-JNK protein expression in hepatic tissues, and reducing the level of insulin in hepatic tissues.
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Coronary artery heart disease (CHD) is one of the common cardiovascular diseases in clinical. The morbidity and mortality of CHD recently continue increasing in our country, which has aroused wide attention. Many studies confirm that traditional Chinese medicine has better therapeutic effect on CHD. Guanxin Danshen formula, widely used in the treatment of CHD, consists of Salviae Miltiorrhizae Radix et Rhizoma, Notoginseng Radix et Rhizoma and volatile oil from Dalbergiae Odoriferae Lignum, and has the efficacy in promoting blood circulation to resolve stasis, regulating the circulation of Qi and alleviating pain. This review summarized the pharmacologic effects and mechanism of Guanxin Danshen formula and its effective components in the treatment of CHD to provide reference for its fundamental research and clinical application.
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The effect of Qizhi Jiangtang vapsule (QJC) on degree of dermal ulcer cicatrization in 2 type diabetic rats was studied. Except the rats for blank group, other male Wistar rats were used to establish type 2 diabetic model by feeding with high sugar and high fat diet for four weeks and intraperitonally injecting with 30 mg•kg⁻¹ streptozotocin (STZ). After that, the rats were divided into balanced groups according to blood sugar, and received corresponding drugs for treatment for 8 weeks. At the end of week 8, 2 cm diameter circular incision was done on the back of rats. After that, the rats were administered continuously for10 days. Area of ulcer surface was detected every two days. After the last administration, wound granulation tissues were cut down to conduct pathological examination and detect the expression of VEGF, PI3K, p-ERK protein in wound tissues. The results showed that compared with the model group, after application of Qizhi Jiangtang capsule (2.24 g•kg⁻¹), the wound was significantly reduced on day 6 and day 10 of wound formation; inflammation reaction on ulcer surface was significantly reduce; Qizhi Jiangtang capsule can increase VEGF expression in the wound tissues of diabetic rats, and inhibit ERK phosphorylation. It can be concluded that Qizhi Jiangtang capsule can promote skin ulcer healing for diabetes rats, and its mechanism may be related to regulating the expression of VEGA and p-ERK proteins.