Search

Background Maintaining proper immune function and hormone status is important for athletes to avoid upper respiratory tract infection (URTI) and insufficient recovery, which is detrimental to sport performance and health. The aim of this study was to evaluate whether three-week supplementation of L-glutamine could benefit the mucosal immunity and hormonal status of combat-sport athletes as well as their rates of upper respiratory tract infection (URTI) and subjective feelings of well-being after intensive training.Methods Twenty-one combat-sport athletes from the National Taiwan University of Sport were recruited in this study. After intensive training, two groups of the participants were asked to consume powder form of 0.3 g/kg body weight of L-glutamine (GLU group) or maltodextrin (PLA group) with drinking water in a randomized design at the same time every day during 3 weeks. Saliva samples were collected to measure immunoglobulin A (IgA), nitric oxide (NO), testosterone (T) and cortisol (C) before and after three-week supplementation; moreover, Hooper’s index questionnaires were completed for wellness assessment. The incidence and duration of URTI were recorded by using a health checklist throughout the entire study period.Results Supplementation of L-glutamine significantly enhanced the concentrations of IgA and NO in saliva; additionally, the incidence of URTI was significantly reduced. Regarding hormones, T concentration was significantly decreased in the PLA group, whereas C concentration was significantly increased, resulting in a significant decrease of T/C ratio. In contrast, the GLU group showed a significant increase of T/C ratio, while the mood scores of the Hooper’s index questionnaire were higher in the PLA group.Conclusions Three-week supplementation of L-glutamine after intensive training enhanced the mucosal immunity, improved hormonal status and reduced the rate of URTI of combat-sport athletes while feelings of well-being were also enhanced. Therefore, L-glutamine would be beneficial for the sports performance and recovery of athletes.

Abstract The COVID‐19 pandemic restricted the regular training and competition program of athletes. Vaccines against COVID‐19 are known to be beneficial for the disease; however, the unknown side effects of vaccines and postvaccination reactions have made some athletes hesitant to get vaccinated. We investigated the changes in inflammatory responses and menstrual cycles of female athletes before and after vaccination. Twenty female athletes were enrolled in this study. Blood was collected from each subject before the first COVID‐19 vaccination and after the first and second vaccinations. Laboratory data, including white blood cell, neutrophil, lymphocyte, and platelet counts, and inflammatory markers, including NLR (neutrophil‐to‐lymphocyte ratio), PLR (platelet lymphocyte ratio), RPR (red cell distribution width to platelet ratio), SII (systemic immune‐inflammation index), and NeuPla (neutrophil–platelet ratio), were analyzed statistically. The menstrual changes before and after vaccination and the side effects were collected by questionnaires. No significant changes in the laboratory data were found after the first and second shots when compared to those at prevaccination: white blood cell, neutrophil, lymphocyte, platelet, NLR, PLR, SII, RPR, and NeuPla (p > 0.05). In addition, there were no significant changes in the menstruation cycle or days of the menstrual period (p > 0.05). All side effects after vaccination were mild and subsided in 2 days. The blood cell counts, inflammatory markers, and menstruation of female athletes were not affected by COVID‐19 vaccines.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used to treat inflammation and pain and even to prevent the progression of cardiovascular disease. They have become widely used because of their effectiveness, especially among athletes performing high-intensity training. Indomethacin is used for pain management in sports medicine and is highly effective and versatile. However, several clinical studies have reported that indomethacin induces acute renal damage. In the present study, we determined that indomethacin reduced human embryonic kidney 293 (HEK293) cell viability in a concentration-dependent manner by triggering apoptosis. In addition, we demonstrated the effect of quercetin on indomethacin-treated HEK293 cells by inactivating the caspase-3 and caspase-9 signals. Furthermore, quercetin reduced ROS production and increased mitochondrial membrane potential (ΔΨm) in indomethacin-treated HEK293 cells. Our results indicate that quercetin can interrupt the activated caspase and mitochondrial pathway induced by indomethacin in HEK293 cells and affect apoptotic mRNA expression. Quercetin can protect against indomethacin-induced HEK293 cell apoptosis by regulating abnormal ΔΨm and apoptotic mRNA expression.

Abstract Background The Campylobacter species usually causes infection between humans and livestock interaction via livestock breeding. The studies of the Campylobacter species thus far in all clinical isolates were to show the many kinds of antibiotic phenomenon that were produced. Their integrons cause the induction of antibiotic resistance between bacterial species in the Campylobacter species. Results The bacterial strains from the diarrhea of pediatric patient which isolated by China Medical University Hospital storage bank. These isolates were identified by MALDI-TOF mass spectrometry. The anti-microbial susceptibility test showed that Campylobacter species resistant to cefepime, streptomycin, tobramycin and trimethoprim/sulfamethoxazole (all C. jejuni and C. coli isolates), ampicillin (89% of C. jejuni; 75% of C. coli), cefotaxime (78% of C. jejuni; 100% of C. coli), nalidixic acid (78% of C. jejuni; 100% of C. coli), tetracycline (89% of C. jejuni; 25% C. coli), ciprofloxacin (67% of C. jejuni; 50% C. coli), kanamycin (33% of C. jejuni; 75% C. coli) and the C. fetus isolate resisted to ampicillin, cefotaxime, nalidixic acid, tetracycline, ciprofloxacin, kanamycin by disc-diffusion method. The effect for ciprofloxacin and tetracycline of the Campylobacter species was tested using an E-test. The tet, erm, and integron genes were detected by PCR assay. According to the sequencing analysis (type I: dfr12-gcuF-aadA2 genes and type II: dfrA7 gene), the cassette type was identified. The most common gene cassette type (type I: 9 C. jejuni and 2 C. coli isolates; type II: 1 C. coli isolates) was found in 12 class I integrase-positive isolates. Conclusions Our results suggested an important information in the latency of Campylobacter species with resistance genes, and irrational antimicrobial use should be concerned.

Idiopathic pulmonary fibrosis accounts for the lethal diffuse fibrosing lung disease, which is described with accumulation of fibroblasts, the loss and damage of lung epithelial cells, and causing respiratory failure. Excessive ROS level impairs the cellular redox level, inflammatory cell infiltration and abnormal collagen production to induce extracellular matrix accumulation. Nuclear factor-erythroid 2 related factor 2 (Nrf2) regulates antioxidant-associated genes as phytochemical target in chemoprevention. The preventive effect of organosulfuric compound diallyl sulfide (DAS) on TGF-β-induced fibrosis in lung MRC-5 fibroblast was investigated in this study. MRC-5 cells were pretreatment with DAS before 10 ng/mL TGF-β stimulation. DAS suppressed the collagen production in TGF-β-induced cells by attenuating Smad 2/3 phosphorylation through activating HO-1 level. DAS inhibited TGF-β-induced myofibroblast formation by decreasing ROS through enhancing Nrf2-related antioxidant enzyme and myofibroblast apoptosis. DAS is a potential dietary agent to inhibit TGF-β-induced fibrosis and to prevent oxidative stress-induced pulmonary fibrosis.

Glucocorticoids are widely used anti-inflammatory drugs in clinical settings. However, they can induce skeletal muscle atrophy by reducing fiber cross-sectional area and myofibrillar protein content. Studies have proven that antioxidants can improve glucocorticoid-induced skeletal muscle atrophy. Quercetin is a potent antioxidant flavonoid widely distributed in fruits and vegetables and has shown protective effects against dexamethasone-induced skeletal muscle atrophy. In this study, we demonstrated that dexamethasone significantly inhibited cell growth and induced cell apoptosis by stimulating hydroxyl free radical production in C2C12 skeletal muscle cells. Our results evidenced that quercetin increased C2C12 skeletal cell viability and exerted antiapoptotic effects on dexamethasone-treated C2C12 cells by regulating mitochondrial membrane potential (ΔΨm) and reducing oxidative species. Quercetin can protect against dexamethasone-induced muscle atrophy by regulating the Bax/Bcl-2 ratio at the protein level and abnormal ΔΨm, which leads to the suppression of apoptosis.

Phyllanthus emblica L. exerts multiple biological functions, and its fruit possesses hepatoprotective benefits. However, the underlying mechanisms of these activities remain unclear. This study aimed to investigate the potential impact of P. emblica on improving nonalcoholic fatty liver disease (NAFLD). Free fatty acid mixture-induced HepG2 cells and leptin-induced HSC-T6 hepatic stellate cells were used to mimic nonalcoholic steatohepatitis and hepatic fibrosis, respectively. Ellagic acid (EA) was identified as a major compound in the water extract of P. emblica fruits (WEPL). WEPL significantly decreased fat accumulation and ROS production by altering lipogenesis-related gene expression and stimulating AMP-activated protein kinase (AMPK) signalling in treated HepG2 cells. WEPL also inhibited hepatic fibrosis in HSC-T6 cells and induced mitochondrial apoptosis. Importantly, EA was shown to inhibit cellular steatosis and liver fibrosis in vitro. In conclusion, WEPL reduces lipogenesis in hepatocytes and fibrotic cells, suggesting that WEPL has the potential to improve NAFLD.

The present study was to explore the biological responses of the newly compound, MJ-29 in murine myelomonocytic leukemia WEHI-3 cells in vitro and in vivo fates. We focused on the in vitro effects of MJ-29 on ER stress and mitochondria-dependent apoptotic death in WEHI-3 cells, and to hypothesize that MJ-29 might fully impair the orthotopic leukemic mice. Our results indicated that a concentration-dependent decrease of cell viability was shown in MJ-29-treated cells. DNA content was examined utilizing flow cytometry, whereas apoptotic populations were determined using annexin V/PI, DAPI staining and TUNEL assay. Increasing vital factors of mitochondrial dysfunction by MJ-29 were further investigated. Thus, MJ-29-provaked apoptosis of WEHI-3 cells is mediated through the intrinsic pathway. Importantly, intracellular Ca(2+) release and ER stress-associated signaling also contributed to MJ-29-triggered cell apoptosis. We found that MJ-29 stimulated the protein levels of calpain 1, CHOP and p-eIF2α pathways in WEHI-3 cells. In in vivo experiments, intraperitoneal administration of MJ-29 significantly improved the total survival rate, enhanced body weight and attenuated enlarged spleen and liver tissues in leukemic mice. The infiltration of immature myeloblastic cells into splenic red pulp was reduced in MJ-29-treated leukemic mice. Moreover, MJ-29 increased the differentiations of T and B cells but decreased that of macrophages and monocytes. Additionally, MJ-29-stimulated immune responses might be involved in anti-leukemic activity in vivo. Based on these observations, MJ-29 suppresses WEHI-3 cells in vitro and in vivo, and it is proposed that this potent and selective agent could be a new chemotherapeutic candidate for anti-leukemia in the future.

Due to the significantly negative impact of the coronavirus (CoV) disease (COVID-19) pandemic on the health of the community and the economy, it remains urgent and necessary to develop a safe and effective treatment method for COVID-19. Huang-LianShang-Qing-Wan (HLSQW) is a herbal formula of traditional Chinese medicine (TCM) that has been applied extensively for treating “wind-heat-associated” symptoms in the upper parts of the body. The objective of the present in silico study was to investigate the potential effects of HLSQW in the context of severe acute respiratory syndrome (SARS)-CoV-2 infection. We analyzed the possible interactions between bioactive compounds within HLSQW on targets that may confer antiviral activity using network pharmacology and pharmacophore-based screening. HLSQW was found to potentially target a number of pathways and the expression of various genes to regulate cell physiology and, consequently, the anti-viral effects against SARS-CoV-2. Bioactive compounds contained within HLSQW may exert combined effects to reduce the production of proinflammatory factors, which may trigger the “cytokine storm” in patients with severe COVID-19. Results from molecular modeling suggested that the bioactive HLSQW components puerarin, baicalin, and daidzin exhibit high binding affinity to the active site of 3-chymotrypsin-like cysteine protease (3CLpro) to form stable ligand-protein complexes, thereby suppressing SARS-CoV-2 replication. In addition, our results also demonstrated protective effects of the HLSQW extract against cell injury induced by the proinflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β, and IL-6, against reactive oxygen species production and nuclear factor-κB activity in normal human lung cells in vitro. To conclude, HLSQW is a potential TCM remedy that warrants further study with the aim of developing an effective treatment for COVID-19 in the future. [ABSTRACT FROM AUTHOR]

Background/Aim: Magnetic resonance imaging (MRI) is a technique for evaluating patients with primary and metastatic tumors. The contrast agents improve the diagnostic accuracy of MRI. Large quantities of a contrast agent must be administrated into the patient to obtain useful images, which leads to cell injury. Gadolinium has been reported to cause central lobular necrosis of the liver and nephrogenic systemic fibrosis. However, the toxicity caused on brain tissue is uncertain. Materials and Methods: This study mainly aimed on the in vitro study of high concentration (2 and 5-fold of normal concentration) gadolinium-based contrast agents (GBCAs), gadodiamide (Omniscan®), on normal brain glial SVG P12 cells. MTT assay, DAPI staining, immunofluorescent staining, [ABSTRACT FROM AUTHOR]

This study investigates the motivations of socially responsible consumption from the perspective of identity-based motivation theory. The findings suggest that personal-identity appeals promote socially responsible products with utilitarian values more effectively than relational-identity appeals. However, with respect to socially responsible products with hedonic values, relational and personal identity had no differential effect. Moreover, public identity appeals were found to promote socially responsible products with utilitarian values significantly. With respect to hedonic products, public identity influenced purchase intention only through anticipated guilt. These results have implications for marketers about ways to promote socially responsible products effectively.

Biliopleural fistula (BF) and formation of biliopleural effusion is a rare complication following percutaneous transhepatic biliary drainage (PTBD). It occurs when the pleura is traversed by the catheter before entering the bile duct. Biliopleural fistula should be suspected when right side pleural effusion develops following the PTBD procedure. The diagnosis of biliopleural fistula is made when greenish pleural fluid with high concentration of bilirubin is aspirated. Here we present a case where a patient develops a biliopleural fistula following PTBD due to obstructive jaundice caused by neuroendocrine tumor of pancreas. Biliopleural fistula was disclosed after a scheduled catheter replacement procedure. Treatments of biliopleural fistula include thoracentesis with drainage tube installation into pleural space. In addition, a drainage tube was installed through percutaneous transhepatic gallbladder drainage (PTGBD) to reduce the bile induced pressure. Surgical repair of fistula was performed after the conservative treatment was unsuccessful. The patient expired 5 days after surgery due to respiratory failure. [ABSTRACT FROM AUTHOR]

Iodinated contrast media (iodinated CM) have increased ability to absorb x-rays and to visualize structures that normally are impossible to observe in a radiological examination. The use of iodinated CM may destory renal function, commonly known as contrast-induced nephropathy (CIN), which can result in acute renal failure (ARF). This review article mainly focuses on the following areas: (1) classifications of iodinated CM: ionic or non-ionic, high-osmolarity contrast media (HOCM), low-osmolarity contrast media (LOCM) and iso-osmolarity contrast media (IOCM); (2) an introduction to the physical and chemical properties of the non-ionic iodinated CM; (3) the management of anaphylactic reaction by iodinated CM; (4) a suggested single injection of adult doses and maximum dose for non-ionic iodinated CM; (5) the molecular mechanism of contrast-induced nephropathy (CIN); (6) In vitro studies on iodinated CM. Based on above information, this review article provide an insight for understanding the drug safety of iodinated CM. [ABSTRACT FROM AUTHOR]

Oral cancer is a serious and fatal disease. Cisplatin is the first line of chemotherapeutic agent for oral cancer therapy. However, the development of drug resistance and severe side effects cause tremendous problems clinically. In this study, we investigated the pharmacologic mechanisms of YC-1 on cisplatin-resistant human oral cancer cell line, CAR. Our results indicated that YC-1 induced a concentration-dependent and time-dependent decrease in viability of CAR cells analyzed by MTT assay. Real-time image analysis of CAR cells by IncuCyte™ Kinetic Live Cell Imaging System demonstrated that YC-1 inhibited cell proliferation and reduced cell confluence in a time-dependent manner. Results from flow cytometric analysis revealed that YC-1 promoted G0/G1 phase arrest and provoked apoptosis in CAR cells. The effects of cell cycle arrest by YC-1 were further supported by up-regulation of p21 and down-regulation of cyclin A, D, E and CDK2 protein levels. TUNEL staining showed that YC-1 caused DNA fragmentation, a late stage feature of apoptosis. In addition, YC-1 increased the activities of caspase-9 and caspase-3, disrupted the mitochondrial membrane potential (ΔΨm) and stimulated ROS production in CAR cells. The protein levels of cytochrome c, Bax and Bak were elevated while Bcl-2 protein expression was attenuated in YC-1-treated CAR cells. In summary, YC-1 suppressed the viability of cisplatin-resistant CAR cells through inhibiting cell proliferation, arresting cell cycle at G0/G1 phase and triggering mitochondria-mediated apoptosis. Our results provide evidences to support the potentially therapeutic application of YC-1 on fighting against drug resistant oral cancer in the future. [ABSTRACT FROM AUTHOR]

Autophagy, a double-edged sword for cell survival, is the research object on 2016 Nobel Prize in Physiology or Medicine. Autophagy is a molecular mechanism for maintaining cellular physiology and promoting survival. Defects in autophagy lead to the etiology of many diseases, including diabetes mellitus (DM), cancer, neurodegeneration, infection disease and aging. DM is a metabolic and chronic disorder and has a higher prevalence in the world as well as in Taiwan. The character of diabetes mellitus is hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance and failure of producing insulin on pancreatic beta cells. In T2DM, autophagy is not only providing nutrients to maintain cellular energy during fasting, but also removes damaged organelles, lipids and miss-folded proteins. In addition, autophagy plays an important role in pancreatic beta cell dysfunction and insulin resistance. In this review, we summarize the roles of autophagy in T2DM. [ABSTRACT FROM AUTHOR]

Tetrandrine has been shown to reduce cancer cell proliferation and to inhibit metastatic effects in multiple cancer models in vitro and in vivo. However, the effects of tetrandrine on the underlying mechanism of HT29 human colorectal adenocarcinoma cell metastasis remain to be fully elucidated. The aim of the present study was focused on tetrandrine-treated HT29 cells following epidermal growth factor (EGF) treatment, and Transwell, gelatin zymography, gene expression and immunoblotting assays were performed to investigate metastatic effects in vitro. Tetrandrine was observed to dose-dependently inhibit EGF-induced HT29 cell invasion and migration, however, no effect on cell viability occurred following exposure to tetradrine between 0.5 and 2 µM. Tetrandrine treatment inhibited the enzymatic activity of matrix metalloprotease (MMP)-2 and MMP-9 in a concentration-dependent manner. The present study also found a reduction in the mRNA expression levels of MMP-2 and MMP-9 in the tetrandrine-treated HT29 cells. Tetrandrine also suppressed the phosphorylation of EGF receptor (EGFR) and its downstream pathway, including phosphoinositide-dependent kinase 1, phosphatidylinositol 3-kinase and phosphorylated AKT, suppressing the gene expression of MMP-2 and MMP-9. Furthermore, tetrandrine triggered mitogen-activated protein kinase signaling through the suppressing the activation of phosphorylated extracellular signal-regulated protein kinase. These data suggested that targeting EGFR signaling and its downstream molecules contributed to the inhibition of EGF-induced HT29 cell metastasis caused by tetrandrine, eventually leading to a reduction in the mRNA and gelatinase activities of MMP-2 and MMP-9, respectively. [ABSTRACT FROM AUTHOR]

Our primary studies had shown that danthron induced cytotoxic effects, including apoptosis and inhibition of migration and invasion. However, danthron-affected DNA damage and repair gene expressions are not clear. In this study, we investigated to examine whether or not danthron induced DNA damage and inhibited DNA repair gene expression in human brain glioblastoma multiforms (GBM 8401) cells. The results from Comet assay indicated that incubation of GBM 8401 cells with 0, 50, 100 and 150 μM of danthron led to a longer DNA migration smear based on the single cell electrophoresis (Comet tail). The results from real-time PCR assay demonstrated that 100 μM of danthron for 24 h treatment in GBM 8401 cells led to decrease all examined ataxia telangiectasia mutated (ATM), ataxia-telangiectasia and Rad3-related (ATR), breast cancer 1, early onset (BRCA-1), 14-3-3 proteins sigma (14-3-3σ), DNA-dependent serine/threonine protein kinase (DNA-PK) and O 6-methylguanine-DNA methyltransferase (MGMT) mRNA expressions. Taken together, the present study showed that danthron caused DNA damage and inhibited DNA repair genes, which may be the factors for danthron-inhibited cell growth in vitro. [ABSTRACT FROM AUTHOR]

Danthron (1,8-dihydroxyanthraquinone), is one of component from Rheum palmatum L. (Polygonaceae), has been shown several biological activities but did not show to induce apoptosis in human brain tumor cells. The aim of this study is to investigate the mechanisms by danthron for the induction of apoptotic potential on human brain glioblastoma multiforms GBM 8401 cell line. Danthron showed a marked concentration- and time-dependent inhibition of GBM 8401 cell viability and induced apoptosis in a dose-and time-dependent manner. There was an attenuation of mitochondrial membrane potential (ΔΨ m) with the alterations of Bcl-2/Bax protein ratio in GBM 8401 cells, indicating the participation of a mitochondria-related mechanism. Pretreatment of a caspase-8 inhibitor (Z-IETD-FMK), caspase-9 inhibitor (Z-LEHD-FMK) and caspase-3 inhibitor (Z-DEVE-FMK) significantly increased the viable of GBM 8401 cells implied that the participations of caspases. Western blotting analysis also showed the activation of initiator caspase-8 and caspase-9, and executor caspase-3 in GBM 8401 cells. Meanwhile, danthron also promoted the generation of reactive oxygen species (ROS) and cytosolic Ca2+ in GBM 8401 cells. Taken together, our data showed that danthron induced apoptosis in GBM 8401 cells through mitochondria-related and caspase-related pathways, and it may be further evaluated as a chemotherapeutic agent for human brain cancer. [ABSTRACT FROM AUTHOR]

Student life causes many sources of stress due to the requirements of managing schoolwork, family, friends, health and wellbeing, and future career planning. Some students are overwhelmed and lack resilience to overcome stress, especially if they are inexperienced in managing setbacks, fail to achieve expectations, or lack skills to independently manage social skills, recreation, and study time. The long-term accumulation of stress has a negative impact on students’ physical and mental health, and may lead to a range of symptoms such as depression, anxiety, headache, insomnia, and eating disorders. Although most universities provide psychological counseling services, there is often a shortage of professional psychologists, which leads to students suffering from stress for longer than necessary without immediate assistance. The build-up of stress can lead to tragic consequences including abnormal reasoning, anti-social behavior, and suicide. There should never be a need for a student to wait more than a month to make an appointment for counseling services and every request for help should be immediately addressed and assessed. In this research, we designed a unique test platform for an immersive virtual reality group chatbot counseling system so students can receive psychological help and stress management counseling anytime and anywhere. First, the research used questionnaires to measure the stress levels and identifies how stress affects their lives. An immersive virtual reality chatbot was developed using professional psychological counseling knowledge that can provide answers during individual or group counseling sessions. Students can log in to the platform as avatars and ask the chatbot questions or interact with other students on the platform. This research provides college students with a new technology-based counseling environment designed to help relieve stress and learn new ways to improve student life quality from others. The platform provides a test base for future clinical trials to evaluate and improve the automated virtual reality chatbot counseling system.

From several decades ago to now, cancer continues to be the leading cause of death worldwide, and metastasis is the major cause of cancer-related deaths. For health benefits, there is a great desire to use non-chemical therapy such as nutraceutical supplementation to prevent pathology development. Over 10,000 different natural bioactives or phytochemicals have been known that possessing potential preventive or supplementary effects for various diseases including cancer. Previously, the in vitro and in vivo anti-invasive and anti-metastatic activities of phenolic acids, monophenol, polyphenol and their derivatives and flavonoids and their derivatives have been reviewed. However, a vast number of natural dietary compounds other than phenolics have been demonstrated to potentially possess the ability to inhibit the invasion and metastasis of various cancers. In this review, we summarize the studies in recent decade on in vitro and in vivo effects and molecular mechanisms of natural bioactives, excluding the phenolics in food, in cancer invasion and metastasis. By combining this review of non-phenolics with the previous phenolics reviews, the puzzle for the contribution of natural dietary bioactives on cancer invasive or/and metastatic progress will be almost complete and more clear. [ABSTRACT FROM AUTHOR]

Rutin, one of the flavonoids, possesses a wide range of biological effects, including antitumor, antioxidant, and anti-inflammatory activities and anti-leukeima cells. Although rutin had been reported to induce apoptosis via caspase-3 activation on human leukemia K562 cells, there is no available information to address whether or not rutin affects leukemia cells in vivo. However, the exact effect of rutin on leukemia cells on murine in vivo is undefined. Therefore, in the present we are focused on the effects of rutin in vivo affecting WEHI-3 cells on murine leukemia. These experiments were divided into 3 parts. Part 1, we examined the effects of rutin on the percentage of viable cells by flow cytometry on WEHI-3 cells in vitro and the results indicated that rutin decreased the viable cells and those effects are dose-and time-dependent effect manners. Part II, we examined the effects of rutin on leukemia WEHI-3 cells in BLAB/c mice in vivo and the results indicated that rutin decreased the percentage of Mac-3 marker, inhibiting the differentiation of precursor of macrophage and T cells which were isolated from spleen. Part III, we examined the size and weight changes of liver and spleen and the results demonstrated that rutin decreased the size and weight of liver and spleen when comparing to the control group. One of the characters of leukemia is the enlarged spleen in murine after i.p. was injected with WEHI-3 cells. Part IV, in the pathological examination, rutin affected the liver and spleen which came from the BLAB/c mice i.p. after injected with WEHI-3 cells treated with or without rutin. Our result showed that rutin affects WEHI-3 cells in vitro and in vivo. [ABSTRACT FROM AUTHOR]

Evidence has accumulated that berberine induced cell cycle arrest and apoptosis in many human cancer cell lines. However, there is no available information to address berberine affecting human oral quamous carcinoma cancer HSC-3 cells. In this study, we have examined the effects of berberine on cell growth and apoptosis and cell cycle regulation in human oral squamous carcinoma HSC-3 cells. Berberine induced dose- and time-dependent of irreversible inhibition of cell growth and cellular DNA synthesis. It was also confirmed by phase-light microscopy which showed that berberine induced morphological changes in HSC-3 cells. Propidium iodide/annexin V staining for flow cytometric analysis showed that berberine induced apoptosis correlating with caspase-3 activation in examined cells. Flow cytometry studies of the cell cycle distribution showed that berberine induced mainly G0/G1-phase arrest. Flow cytometry examinations also showed that berberine induced reactive oxygen species (ROS) and Ca2+ production and dysfunction of mitochondrial membrane potential (MMP) which are correlated with apoptosis. In conclusion, our data supports a view that berberine initially induces an endoplasmic reticulum stress response based on ROS and Ca2+ production then followed by dysfunction mitochondria, resulting in apoptosis of these oral cancer HSC-3 cells. Prolonged exposure of the HSC-3 cells to berberine causes increased percentage of apoptosis through decreased levels of MMP, cytochrome c release and activation of caspase-3. [ABSTRACT FROM AUTHOR]

The triggering of gemcitabine (GEM) drug resistance in pancreatic cancer by the receptor for advanced glycation end products (RAGE) has been demonstrated. Hence, finding a safe and effective adjuvant for preventing pancreatic cancer progression is imperative. Quercetin is a flavonoid that is abundant in apples, grapes, red raspberry, and onions and has been reported to inhibit RAGE. This research aimed to investigate the mechanisms of quercetin in regulating cell death and enhancing drug effects through RAGE reduction, especially in GEM-resistant pancreatic cancer cells. Our results showed that silencing RAGE expression by RAGE-specific siRNA transfection significantly increased cell death by apoptosis, autophagy and GEM-induced cytotoxicity by suppressing the PI3K/AKT/mTOR axis in MIA Paca-2 and MIA Paca-2 GEMR cells (GEM-resistant cells). Notably, quercetin showed a dramatic effect similar to RAGE silencing that effectively attenuated RAGE expression to facilitate cell cycle arrest, autophagy, apoptosis, and GEM chemosensitivity in MIA Paca-2 GEMR cells, suggesting that an additional reaction occurred under combined quercetin and GEM treatment. In conclusion, the results demonstrated that the molecular mechanisms of quercetin in regulating apoptosis and autophagy-related pathways and increasing GEM chemosensitivity in pancreatic cancer cells involved inhibition of RAGE expression. [ABSTRACT FROM AUTHOR]