Oral Chinese Herbal Medicine plus usual care for diabetic kidney disease: study protocol for a randomized, double-blind, placebo-controlled pilot trial.

Background: Diabetic kidney disease (DKD) has become the leading cause of kidney failure, causing a significant socioeconomic burden worldwide. The usual care for DKD fails to achieve satisfactory effects in delaying the persistent loss of renal function. A Chinese herbal medicine, Tangshen Qushi Formula (TQF), showed preliminary clinical benefits with a sound safety profile for people with stage 2-4 DKD. We present the protocol of an ongoing clinical trial investigating the feasibility, efficacy, and safety of TQF compared to placebo in delaying the progressive decline of renal function for people with stage 2-4 DKD. Methods: A mixed methods research design will be used in this study. A randomized, double-blind, placebo-controlled pilot trial will evaluate the feasibility, efficacy, and safety of TQF compared to placebo on kidney function for people with stage 2-4 DKD. An embedded semi-structured interview will explore the acceptability of TQF granules and trial procedures from the participant's perspective. Sixty eligible participants with stage 2-4 DKD will be randomly allocated to the treatment group (TQF plus usual care) or the control group (TQF placebo plus usual care) at a 1:1 ratio for 48-week treatment and 12-week follow-up. Participants will be assessed every 12 weeks. The feasibility will be assessed as the primary outcome. The changes in the estimated glomerular filtration rate, urinary protein/albumin, renal function, glycemic and lipid markers, renal composite endpoint events, and dampness syndrome of Chinese medicine will be assessed as the efficacy outcomes. Safety outcomes such as liver function, serum potassium, and adverse events will also be evaluated. The data and safety monitoring board will be responsible for the participants' benefits, the data's credibility, and the results' validity. The intent-to-treat and per-protocol analysis will be performed as the primary statistical strategy. Discussion: Conducting a rigorously designed pilot trial will be a significant step toward establishing the feasibility and acceptability of TQF and trial design. The study will also provide critical information for future full-scale trial design to further generate new evidence supporting clinical practice for people with stage 2-4 DKD. Trial registration number: https://www.chictr.org.cn/, identifier ChiCTR2200062786.

Mechanism of apoptotic induction on T24 cells by honokiol and its synergistic anticancer effect in combination with hydroxycamptothecin.

OBJECTIVE: To investigate the mechanism of honokiol (HNK) on bladder cancer cells and its synergistic anticancer effect with hydroxycamptothecin (HCPT). METHODS: Control, HNK, HCPT, and HNK plus HCPT groups were established. The morphological characteristics of T24 cells were examined microscopically. The maximal experimental concentration of HNK and HCPT were determined according to IC10 detected by MTT. T24 cell viability and the percentage of apoptotic cells were assessed on the basis of MTT and flow cytometric analysis. The expression of caspase-3, caspase-9, phosphorylated nuclear factor-kappa B (NF-κB)-p65, Akt, and extracellular signal-regulated kinase (ERK) proteins were analyzed by Western blot. RESULTS: Apoptosis in T24 cells was observed microscopically in both the HNK and HCPT groups and even more obvious in the HNK plus HCPT groups. The percentage of T24 cell viability decreased down to 19.41% , and the percentage of apoptotic cells rose to 54.08% when treated with HNK plus HCPT in an HNK dose-dependent manner. The induction of caspase-3 and caspase-9 proteins and the inhibition of phosphorylation of NF-κB-p65, Akt, and ERK proteins in T24 cells were demonstrated in the HNK groups, and more significantly in the HNK plus HCPT groups, but not in the HCPT group. CONCLUSION: The anticancer effect of HNK may be due to the activation of the caspase pathway and inhibition of phosphorylation of NF-κB, Akt, and ERK. HNK in combination with HCPT produces a synergistic cell-killing effect on bladder cancer cells.

HINT1 (Histidine Triad Nucleotide-Binding Protein 1) Attenuates Cardiac Hypertrophy Via Suppressing HOXA5 (Homeobox A5) Expression.

BACKGROUND: Cardiac hypertrophy is an important prepathology of, and will ultimately lead to, heart failure. However, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown. This study aims to elucidate the effects and mechanisms of HINT1 (histidine triad nucleotide-binding protein 1) in cardiac hypertrophy and heart failure. METHODS: HINT1 was downregulated in human hypertrophic heart samples compared with nonhypertrophic samples by mass spectrometry analysis. Hint1 knockout mice were challenged with transverse aortic constriction surgery. Cardiac-specific overexpression of HINT1 mice by intravenous injection of adeno-associated virus 9 (AAV9)-encoding Hint1 under the cTnT (cardiac troponin T) promoter were subjected to transverse aortic construction. Unbiased transcriptional analyses were used to identify the downstream targets of HINT1. AAV9 bearing shRNA against Hoxa5 (homeobox A5) was administrated to investigate whether the effects of HINT1 on cardiac hypertrophy were HOXA5-dependent. RNA sequencing analysis was performed to recapitulate possible changes in transcriptome profile.Coimmunoprecipitation assays and cellular fractionation analyses were conducted to examine the mechanism by which HINT1 regulates the expression of HOXA5. RESULTS: The reduction of HINT1 expression was observed in the hearts of hypertrophic patients and pressure overloaded-induced hypertrophic mice, respectively. In Hint1-deficient mice, cardiac hypertrophy deteriorated after transverse aortic construction. Conversely, cardiac-specific overexpression of HINT1 alleviated cardiac hypertrophy and dysfunction. Unbiased profiler polymerase chain reaction array showed HOXA5 is 1 target for HINT1, and the cardioprotective role of HINT1 was abolished by HOXA5 knockdown in vivo. Hoxa5 was identified to affect hypertrophy through the TGF-ß (transforming growth factor ß) signal pathway. Mechanically, HINT1 inhibited PKCß1 (protein kinase C ß type 1) membrane translocation and phosphorylation via direct interaction, attenuating the MEK/ERK/YY1 (mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/yin yang 1) signal pathway, downregulating HOXA5 expression, and eventually attenuating cardiac hypertrophy. CONCLUSIONS: HINT1 protects against cardiac hypertrophy through suppressing HOXA5 expression. These findings indicate that HINT1 may be a potential target for therapeutic interventions in cardiac hypertrophy and heart failure.

Yin Yang 1 protein ameliorates diabetic nephropathy pathology through transcriptional repression of TGFß1.

Transforming growth factor-ß1 (TGFß1) has been identified as a major pathogenic factor underlying the development of diabetic nephropathy (DN). However, the current strategy of antagonizing TGFß1 has failed to demonstrate favorable outcomes in clinical trials. To identify a different therapeutic approach, we designed a mass spectrometry-based DNA-protein interaction screen to find transcriptional repressors that bind to the TGFB1 promoter and identified Yin Yang 1 (YY1) as a potent repressor of TGFB1. YY1 bound directly to TGFB1 promoter regions and repressed TGFB1 transcription in human renal mesangial cells. In mouse models, YY1 was elevated in mesangial cells during early diabetic renal lesions and decreased in later stages, and knockdown of renal YY1 aggravated, whereas overexpression of YY1 attenuated glomerulosclerosis. In addition, although their duration of diabetic course was comparable, patients with higher YY1 expression developed diabetic nephropathy more slowly compared to those who presented with lower YY1 expression. We found that a small molecule, eudesmin, suppressed TGFß1 and other profibrotic factors by increasing YY1 expression in human renal mesangial cells and attenuated diabetic renal lesions in DN mouse models by increasing YY1 expression. These results suggest that YY1 is a potent transcriptional repressor of TGFB1 during the development of DN in diabetic mice and that small molecules targeting YY1 may serve as promising therapies for treating DN.

[Enhancement for Anaerobic Digestion of Waste Activated Sludge Based on Microwave Pretreatment Combined with Zero Valent Iron].

In this study, we investigated the enhanced performance after addition of zero valent iron (ZVI) under different dosages (low range of 5.19-41.51 g·kg-1 TS and high range of 83.35-853.46 g·kg-1 TS), combined with microwave (MW) pretreatment for anaerobic digestion (AD) of waste activated sludge (WAS). The results demonstrated that the methane production potential of WAS could be increased by 17%-24% with the addition of ZVI combined with MW pretreatment, and especially the methane production rate was enhanced in the initial days (1-4d). ZVI addition could further improve the enhanced performance of AD under MW pretreatment. Compared with the performance of AD with only MW pretreatment, the methane production potential was increased by 7.42%, and methane production flow rate at 2 d was increased by 11.02% with 31.13 g·kg-1 TS of ZVI addition. However, the higher dosage of added ZVI did not show further enhanced performance. It was concluded that ZVI addition promoted the release of dissolved organics at the initial stage of AD. For instance, soluble proteins were increased by 21.16% with the ZVI addition of 31.13 g·kg-1 TS compared with pretreated WAS without ZVI addition. Furthermore, ZVI addition accelerated the degradation of acetic acid, iso-butyric acid, and iso-valeric acid, and led to a significant reduction of orthophosphate and sulfate in the supernatant of the digested sludge. The concentration of iron in the supernatant decreased even with a high dosage of ZVI. Thus, the formation of precipitate that occurred due to reactions between iron and orthophosphate or sulfate, may be the main reason for the lack of enhanced performance even with high dosage of ZVI addition.

Efficacy and Safety of Serenoa repens Extract Among Patients with Benign Prostatic Hyperplasia in China: A Multicenter, Randomized, Double-blind, Placebo-controlled Trial.

OBJECTIVE: To evaluate the efficacy and safety of Serenoa repens among patients with benign prostatic hyperplasia (lower urinary tract symptoms/benign prostatic hyperplasia [LUTS/BPH]) in China. METHODS: We conducted a double blind, placebo-controlled study of 354 patients with LUTS/BPH from 19 institutions, to evaluate the efficacy and safety of Serenoa repens. Participants were randomly assigned (1:1) into the Serenoa repens extract (320 mg) or placebo groups for 24 weeks. Primary efficacy parameters were changes in International Prostate Symptom Score and peak urinary flow from baseline to each assessment. Secondary efficacy parameters included improvement of storage symptom and voiding symptom scores, prostate volume, urinary frequency, and total prostate-specific antigen level. Other parameters assessed were quality of life score, a four-item male sexual function questionnaire score, and International Index of Erectile Function score across the consecutive double-blind visits. RESULTS: Statistically significant improvement in the peak urinary flow, International Prostate Symptom Score, scores of storage symptoms and voiding symptoms, quality of life score, four-item male sexual function questionnaire score, and International Index of Erectile Function score were observed in the Serenoa repens extract group compared with those in the placebo group (P <.05). Two (1.18%) of 169 patients in the placebo group and 3 (1.89) of 159 patients in the Serenoa repens extract group experienced 1 or more adverse events. CONCLUSION: The Serenoa repens extract was effective, safe, well-tolerated, and clinically and statistically superior to placebo in the target LUTS/BPH population.

Trends in Treatment for Prostate Cancer in China: Preliminary Patterns of Care Study in a Single Institution.

Objectives: A Patterns of Care Study (PCS) was performed in the largest regional medical center in Zhejiang Province, China. The hospital information system (HIS) was used to evaluate patient characteristics and changes in initial treatment patterns for prostate cancer and to determine recent predominant trends in treatment plans for prostate cancer (PCa) in China. Methods: Men who were newly diagnosed with localized or locally advanced PCa for 2010-2011 and 2016-2017 were identified in the HIS database. Patient characteristics and temporal trends in initial management were assessed, and differences between groups were evaluated for significance using Chi-square and Mann-Whitney U tests. Results: In total, 1792 patients met the study criteria, including 505 and 1287 patients in the 2010-2011 and 2016-2017 samples, respectively. The average age of patients diagnosed in the 2010-2011 PCS survey was 70 years, decreasing to 68 years when the 2016-2017 patients were included (P<0.001). In the 2010-2011 sample, 50.69% of the patients had an initial prostate-specific antigen (PSA) level ≥20 ng/ml. In contrast, the initial PSA level was 4-19.99 ng/ml for 66.67% of the patients in the 2016-2017 sample (P<0.001). Based on National Comprehensive Cancer Network (NCCN) criteria, the percentages of patients in low- and intermediate-risk groups increased from 33.06% to 54.78%; conversely, the percentages in high-risk, very high-risk, and regional (N1) groups decreased to a certain extent (P<0.001). According to European Association of Urology (EAU) criteria, the percentages of patients in low- and intermediate-risk groups increased from 32.07% to 53.69%, yet the percentage in the high-risk group decreased (P<0.001). The use of radical prostatectomy (RP) and radiation therapy (RT) increased from 48.32% to 76.46% and 5.35% to 16.94%, particularly in high-risk and low-risk groups, respectively, whereas the rates of hormone therapy (HT) and active surveillance and observation (AS&O) decreased from 32.28% to 4.27% and from 16.04% to 2.33%, respectively (P<0.001). A similar pattern was observed when patients were stratified by EAU risk group. Conclusions: The results of this real-world study in the largest regional medical center in Zhejiang Province, China, indicate that the predominant characteristics of PCa patients and trends in initial management are changing rapidly. We found the following: (a) a trend toward a decreased age among newly diagnosed patients; (b) a trend toward lower initial PSA levels; (c) a downward trend in risk group classification; (d) a significant increase in the likelihood of receiving RP, particularly in the high-risk group; (e) an increase in the rate of RP, mostly due to use of the Da Vinci robotic system; (f) a significant increase in the likelihood of receiving RT, especially in the low-risk group; and (g) a decrease in HT and AS&O.

fam20C participates in the shell formation in the pearl oyster, Pinctada fucata.

Kinase-family with sequence similarity 20, member C (Fam20C) is a protein kinase, which can phosphorylate biomineralization related proteins in vertebrate animals. However, the function of Fam20C in invertebrate animals especially the role in biomineralization is still unknown. Herein, we cloned the cDNA of fam20C from the pearl oyster, Pinctada fucata. It is showed that the expression of fam20C in the mantle edge was much higher than other tissues. In situ hybridization showed that fam20C was expressed mostly in the outer epithelial cells of the middle fold, indicating it may play important roles in the shell formation. Besides, fam20C expression increased greatly in the D-shape stage of pearl oyster development, when the shell was first formed. During the shell repair process, the expression level of fam20C increased 1.5 times at 6 h after shell notching. Knockdown of fam20C in vivo by RNA interference resulted in abnormally stacking of calcium carbonate crystals at the edges of nacre tablets, showing direct evidence that fam20C participates in the shell formation. This study provides an insight into the role of kinase protein in the shell formation in mollusk and broaden our understanding of biomineralization mechanism.

Phenolic constituents from Alisma plantago-aquatica Linnaeus and their anti-chronic prostatitis activity.

BACKGROUND: The plant Alisma plantago-aquatica Linnaeus, which is widely distributed in southwest of China, is the main material of traditional Chinese medicine "Zexie". It was used as folk medicine for immune-modulation, anti-tumor, anti-inflammatory and antibacterial. Previous chemical studies on A. plantago-aquatica reported the identification of triterpenes, diterpenes, sesquiterpenes, steroids, alkaloids and phenolic acid. Terpenes and phenolic acid were regard as major secondary metabolites from this medicine plant. RESULTS: A new phenolic acid, plantain A (1), along with four known compounds (2-5) were isolated and identified from A. plantago-aquatica by extensive chromatographic and spectrometric methods. In the present study, the levels of TNF-α, IL-1ß, COX-2, PEG2 and TGF-ß1 were increased in model group rats, whereas on treatment with the isolated compound (1 and 4) at 50 mg/kg, there was a significant decrease in the cytokine levels. Therefore, the anti-CNP effect of 1 and 4 may be related to their anti-inflammatory properties. CONCLUSIONS: A new phenolic acid and four known phenolic compounds were isolated from A. plantago-aquatica. Moreover, compounds 1 and 4 shows significant anti-chronic prostatitis activity in rats.

A Novel Matrix Protein, PfY2, Functions as a Crucial Macromolecule during Shell Formation.

Biomineralization, including shell formation, is dedicatedly regulated by matrix proteins. PfY2, a matrix protein detected in the ethylene diamine tetraacetic acid (EDTA)-soluble fraction from both prismatic layer and nacreous layer, was discovered by our group using microarray. It may play dual roles during biomineralization. However, the molecular mechanism is still unclear. In this research, we studied the function of PfY2 on crystallization in vivo and in vitro, revealing that it might be a negative regulator during shell formation. Notching experiment indicated that PfY2 was involved in shell repairing and regenerating process. Repression of PfY2 gene affected the structure of prismatic and nacreous layer simultaneously, confirming its dual roles in shell formation. Recombinant protein rPfY2 significantly suppressed CaCO3 precipitation rate, participated in the crystal nucleation process, changed the morphology of crystals and inhibited the transformation of amorphous calcium carbonate (ACC) to stable calcite or aragonite in vitro. Our results may provide new evidence on the biomineralization inhibition process.

Jolkinolide A and Jolkinolide B Inhibit Proliferation of A549 Cells and Activity of Human Umbilical Vein Endothelial Cells.

BACKGROUND Jolkinolide A (JA) and Jolkinolide B (JB) are diterpenoids extracted from the roots of Euphorbia fischeriana Steud and have been shown to have anti-tumor activity. However, their effects on the ability of tumor cells to invade blood vessels and metastasize remain largely unknown. Investigations into the effects of JA and JB on the angiogenesis of tumor tissues may facilitate the identification of new natural drugs with anti-tumor growth and metastasis activities. MATERIAL AND METHODS We used different concentrations of JA and JB (20 µg/ml, 40 µg/ml, 60 µg/ml, 80 µg/ml, and 100 µg/ml) to stimulate A549 cells and then studied the effects on the growth and metastasis of lung cancers. In addition, we used conditional media from A549 cells (A549-CM) stimulated by either JA or JB in different concentrations to culture human umbilical vein endothelial cells (HUVECs). RESULTS We found that both JA and JB significantly inhibited the Akt-STAT3-mTOR signaling pathway and reduced the expression of VEGF in A549 cells, but JB exhibited more significant inhibitory effects than JA. The JB-stimulated A549 cell conditional media had a greater inhibitory effect on the proliferation and migration of HUVECs than did the conditional media of JA-stimulated A549 cells. This effect gradually increased with increasing concentrations of either type of Jolkinolide. CONCLUSIONS Our results suggest that JA and JB inhibited VEGF expression in A549 cells through the inhibition of the Akt-STAT3-mTOR signaling pathway, and directly inhibited the proliferation and migration of HUVECs. These findings are of great significance for the development of new plant-derived chemotherapy agents for the treatment of cancer.

Anti-proliferative and apoptotic effects of S1, a tetrandrine derivative, in human gastric cancer BGC-823 cells.

The aim of the study was to investigate the anti-proliferation and apoptosis-inducing effects of S1, a novel tetrandrine derivative, in human gastric cancer BGC-823 cells and explore the possible mechanism of action. The anti-proliferative activity was determined by MTT assay; the induction of cell cycle arrest and apoptosis were detected by flow cytometry. Quantitative real time RT-PCR and Western blotting were used to evaluate the mRNA and protein expression levels in mitochondrial pathway. S1 significantly reduced cell viability and induced a G2/M phase arrest and apoptosis in dose- and time-dependent manner. Further studies showed that S1 increased mRNA and protein expression of Bax and the Bax/Bcl-2 ratio. Moreover, S1 decreased the protein expression of procaspase-9 and procaspase-3, suggesting that the induction of apoptosis may be related to the alteration of the ratio of Bax/Bcl-2 and the activation of caspases. These findings suggested that S1 merits further investigation as a novel therapeutic agent for the treatment of human gastric cancer.

The AP-1 transcription factor homolog Pf-AP-1 activates transcription of multiple biomineral proteins and potentially participates in Pinctada fucata biomineralization.

Activator protein-1 (AP-1) is an important bZIP transcription factor that regulates a series of physiological processes by specifically activating transcription of several genes, and one of its well-chartered functions in mammals is participating in bone mineralization. We isolated and cloned the complete cDNA of a Jun/AP-1 homolog from Pinctada fucata and called it Pf-AP-1. Pf-AP-1 had a highly conserved bZIP region and phosphorylation sites compared with those from mammals. A tissue distribution analysis showed that Pf-AP-1 was ubiquitously expressed in P. fucata and the mRNA level of Pf-AP-1 is extremely high in mantle. Pf-AP-1 expression was positively associated with multiple biomineral proteins in the mantle. The luciferase reporter assay in a mammalian cell line showed that Pf-AP-1 significantly up-regulates the transcriptional activity of the promoters of KRMP, Pearlin, and Prisilkin39. Inhibiting the activity of Pf-AP-1 depressed the expression of multiple matrix proteins. Pf-AP-1 showed a unique expression pattern during shell regeneration and pearl sac development, which was similar to the pattern observed for biomineral proteins. These results suggest that the Pf-AP-1 AP-1 homolog is an important transcription factor that regulates transcription of several biomineral proteins simultaneously and plays a role in P. fucata biomineralization, particularly during pearl and shell formation.

Cloning and identification of a YY-1 homolog as a potential transcription factor from Pinctada fucata.

Biomineralization is an important and ubiquitous process in organisms. The shell formation of mollusks is a typical biomineral physical activity and is used as a canonical model in biomineralization research. Most recent studies focused on the identification of matrix proteins involved in shell formation; however, little is known about their transcriptional regulation mechanism, especially the transcription factors involved in shell formation. In this study, we identified a homolog of the YY-1 transcriptional factor from Pinctada fucata, named Pf-YY-1, and characterized its expression pattern and biological functions. Pf-YY-1 has a typical zinc finger motif highly similar to those in humans, mice, and other higher organisms, which indicated its DNA-binding capability and its function as a transcription factor. Pf-YY-1 is ubiquitously expressed in many tissues, but at a higher level in the mantle, which suggested a role in biomineralization. The expression pattern of Pf-YY-1 during pearl sac development was quite similar to, and was synchronized with, those of Prisilkin-39, ACCBP, and other genes involved in biomineralization, which also suggested its function in biomineralization.

cfMSP-1, an extremely acidic matrix protein involved in shell formation of the scallop Chlamys farreri.

Matrix proteins play an important role in biomineralization by mollusks. In this study, we cloned and characterized an acidic protein (pI=3.36) homolog of cfMSP-1 that is highly expressed in the mantle transcriptome of the scallop Chlamys farreri. RT-PCR and in situ hybridization showed that cfMSP-1 is specifically expressed in the outer fold of the mantle edge and pallial part. The expression level of cfMSP-1 remarkably increased and then reduced gradually to a value that is ~2-fold higher than basal levels after shell notching. Knock-down expression of cfMSP-1 in adults via dsRNA injection gave a disordered folia surface. Both shell notching and RNAi experiments indicated that cfMSP-1 plays an essential role in the formation of the folia of C. farreri.

Acthi, a thiazole biosynthesis enzyme, is essential for thiamine biosynthesis and CPC production in Acremonium chrysogenum.

BACKGROUND: The filamentous fungus Acremonium chrysogenum is an important industrial fungus and is used in the production of the ß-lactam antibiotic cephalosporin C. Little is known regarding the molecular and biological mechanisms of how this industrial strain was improved by mutagenesis and molecular breeding. Comparative proteomics is one of the most powerful methods to evaluate the influence of gene expression on metabolite production. RESULTS: In this study, we used comparative proteomics to investigate the molecular mechanisms involved in the biosynthesis of cephalosporin C between a high-producer (HY) strain and a wide-type (WT) strain. We found that the expression levels of thiamine biosynthesis-related enzymes, including the thiazole biosynthesis enzyme (Acthi), pyruvate oxidase, flavin adenine dinucleotide (FAD)-dependent oxidoreductase and sulfur carrier protein-thiS, were up-regulated in the HY strain. An Acthi-silencing mutant of the WT strain grew poorly on chemically defined medium (MMC) in the absence of thiamine, and its growth was recovered on MMC medium supplemented with thiamine. The intracellular thiamine content was changed in the Acthi silencing or over-expression mutants. In addition, we demonstrated that the manipulation of the Acthi gene can affect the hyphal growth of Acremonium chrysogenum, the transcription levels of cephalosporin C biosynthetic genes, the quantification levels of precursor amino acids for cephalosporin C synthesis and the expression levels of thiamine diphosphate-dependent enzymes. Over-expression of Acthi can significantly increase the cephalosporin C yield in both the WT strain and the HY mutant strain. CONCLUSIONS: Using comparative proteomics, four differently expressed proteins were exploited, whose functions may be involved in thiamine diphosphate metabolism. Among these proteins, the thiazole biosynthesis enzyme (ActhiS) may play an important role in cephalosporin C biosynthesis. Our studies suggested that Acthi might be involved in the transcriptional regulation of cephalosporin C biosynthesis. Therefore, the thiamine metabolic pathway could be a potential target for the molecular breeding of this cephalosporin C producer for industrial applications.

Tea consumption and prostate cancer: an updated meta-analysis.

OBJECTIVES: Tea is supposed to have chemopreventive effect against various cancers. However, the protective role of tea in prostate cancer is still controversial. The aim of this study is to elucidate the association between tea consumption and prostate cancer risk by meta-analysis. METHODS: A total of 21 published articles were retrieved via both computerized searches and review of references. Estimates of OR/RR for highest versus non/lowest tea consumption levels were pooled on the basis of random effect model or fixed effect model as appropriate. Stratified analyses on tea type, population and study design were also conducted. RESULTS: No statistical significance was detected between tea consumption and prostate cancer risk in meta-analysis of all included studies (odds ratio (OR) = 0.86, 95% CI (0.69-1.04)). Furthermore, stratified analyses on population (Asian, OR = 0.81, 95% CI (0.55-1.08); non-Asian, OR = 0.89, 95% CI (0.72-1.07)) and tea type (green tea, OR = 0.79, 95% CI (0.43-1.14); black tea, OR = 0.88, 95% CI (0.73-1.02)) also yielded non-significant association. Only the case-control study subgroup demonstrated a borderline protective effect for tea consumption against prostate cancer (OR = 0.77, 95% CI (0.55-0.98)). CONCLUSION: Our analyses did not support the conclusion that tea consumption could reduce prostate cancer risk. Further epidemiology studies are needed.

[Preventive effects of jinghua weikang capsule on NSAID-induced injury to the mucosa of the small intestine: an experimental research].

OBJECTIVE: To study the preventive effects of jinghua weikang capsule (JWC) on nonsteroidal anti-inflammatory drugs (NSAIDs) induced injury to the mucosa of the small intestine. METHODS: Thirty-two Wistar rats were randomly divided into four groups, i.e., the blank control group, the model group, the JWC group, and the esomeprazole group. Diclofenac was administered to rats in the model group, the JWC group, and the esomeprazole group at the daily dose of 15 mg/kg. JWC and esomeprazole was respectively given to those in the JWC group, and the esomeprazole group one day ahead. Normal saline was given to rats in the blank control group. Rats were killed 3 days later. The pathological changes of the small intestine were observed by hematoxylin and eosin stain. RESULTS: Compared with the blank control group, the general score for the small intestine (4.63 +/-0.52 vs 0.00 +/-0. 00) and the pathological score (4.00 +/-0.90 vs 0.00 +/-0. 00) obviously increased in the model group, showing statistical difference (P <0.05). Compared with the model group, the general score for the small intestine (1.88 +/-0.99) and the pathological score (2.11 +/-1.11) obviously decreased in the JWG group, showing statistical difference (P <0.05). Compared with the model group, the general score for the small intestine (2.75 +/-1.28) and the pathological score (2. 30 +/-0.94) obviously decreased in the esomeprazole group, showing statistical difference (P <0.05). CONCLUSION: JWC could prevent NSAIDs induced injury to the mucosa of the small intestine.

No association between tea consumption and risk of renal cell carcinoma: a meta-analysis of epidemiological studies.

OBJECTIVE: To evaluate the association between tea consumption and the risk of renal cell carcinoma. METHODS: We searched PubMed,Web of Science and Scopus between 1970 and November 2012. Two evaluators independently reviewed and selected articles based on predetermined selection criteria. RESULTS: Twelve epidemiological studies (ten case-control studies and two cohort studies) were included in the final analysis. In a meta-analysis of all included studies, when compared with the lowest level of tea consumption, the overall relative risk (RR) of renal cell carcinoma for the highest level of tea consumption was 1.03 (95% confidence interval [CI] 0.89-1.21). In subgroup meta-analyses by study design, there was no significant association between tea consumption and renal cell carcinoma risk in ten case-control studies using adjusted data (RR=1.08, 95% CI 0.84-1.40). Furthermore, there was no significant association in two cohort studies using adjusted data (RR=0.95, 95% CI 0.81-1.12). CONCLUSION: Our findings do not support the conclusion that tea consumption is related to decreased risk of renal cell carcinoma. Further prospective cohort studies are required.

A meta-analysis of tea consumption and the risk of bladder cancer.

OBJECTIVE: Previous studies on the association between tea consumption and bladder cancer risk have only illustrated contradictory results. The role of tea in bladder carcinogenesis still remains conflicting. In order to illustrate the potential relationship between tea consumption and bladder cancer, a meta-analysis of case-control and cohort studies was conducted. METHODS: Eligible studies were retrieved via both computerized searches and review of references. Stratified analyses on types of tea, gender, study design, ethnicity and smoking status were performed. Fixed- or random-effect models were used to summarize the estimates of OR with 95% CIs. RESULTS: Seventeen studies were eligible for our analysis. No statistical significance was detected between tea consumption and bladder cancer risk when comparing the highest with the lowest intake of tea (OR = 0.825, 95% CI 0.652-1.043). In the subgroup of green tea, we observed it illustrated a protective effect on bladder cancer (OR = 0.814, 95% CI 0.678-0.976). CONCLUSION: Our analysis indicated that green tea may have a protective effect on bladder cancer in Asian people. Further studies need to be conducted to better clarify the biological mechanisms.