The effects of apple cider vinegar on cardiometabolic risk factors: A systematic review and meta-analysis of clinical trials.

BACKGROUND: Cardiometabolic syndrome (CMS) is a set of metabolic abnormalities that are risk factors for cardiovascular disease (CVD). Apple cider vinegar (ACV) has been used in several studies as a natural agent to improve CMS risk factors. The present study aimed to perform a systematic review and meta-analysis of the effects of ACV consumption on lipid and glycemic parameters. METHODS: PubMed, Scopus, and ISI Web of Science databases were systematically searched to find clinical trials evaluating the effects of ACV consumption on CMS risk factors. RESULTS: Overall, 25 clinical trials (33 arms) comprising 1320 adults were entered in this study. ACV consumption could significantly improve the levels of FBG (-21.20 mg/dl; 95% CI: -32.31 to -2.21; I2: 95.8%), HbA1c (-0.91mg/dl; 95% CI: -1.62 to -0.21; I2: 98.9%), and TC (-6.72 mg/dl; 95% CI: -12.91 to -0.53; I2:50.8%). No significant results were observed for BMI, HOMA-IR, serum insulin, TG, LDL-C, and HDL-C. Subgroup analysis showed a significant decrease in FBG, HbA1c, TC, and TG in diabetic patients. In this type of analysis, ACV consumption significantly reduced FBG levels when administered for both duration subgroups (≥12 and <12 weeks). Moreover, in the subgroup analysis based on duration, TG concentration was significantly decreased following ACV consumption for ≥ 12 weeks. CONCLUSION: This meta-analysis showed that consumption of ACV has a favorable effect in decreasing some CMS risk factors including FBG, HbA1c, and TC.

Effect of citalopram and sertraline on the expression of miRNA- 124, 132, and 16 and their protein targets in patients with depression.

Objectives: This study aimed to evaluate the effect of SSRIs on the expression of miRNAs and their protein targets. Materials and Methods: In a 100 day open-label study of citalopram (n=25) and sertraline (n=25), levels of miRNA 16, 132, and 124 and glucocorticoid receptor (GR), Brain-derived neurotrophic factor (BDNF), and serotonin transporter (SERT) protein expression were measured by QRT-PCR and western blot in healthy control (n=20), patients with depression at the baseline, and same patients after 100 days of treatment. Results: Expression levels of GR and BDNF proteins were lower in the depressed group before treatment as compared with the healthy group (P<0.0001). The SERT level was higher among the depressed group before treatment in comparison with the healthy group (P<0.0001). The level of GR and BDNF significantly increased, and SERT expression decreased after receiving sertraline (P<0.05). When the depressed group received citalopram, only SERT and GR were altered (P<0.05). Among the microRNAs' expression investigated, mir-124 and mir-132 were higher, and mir-16 was lower among the depressed compared with the healthy group (P<0.0001). Individuals receiving citalopram only showed an increase in the expression of mir-16 while administration of sertraline led to a significant increase in the expression of mir-16 and a decrease in mir-124 and mir-132 (P<0.05). Conclusion: This elucidated the relationship between antidepressant treatment and the expression of different microRNA that control gene expression in various pathways involved in depressed patients. Receiving SSRI can affect the level of these proteins and their relevant microRNAs.

The effects of curcumin on Brain-Derived Neurotrophic Factor expression in neurodegenerative disorders.

Brain-Derived Neurotrophic Factor (BDNF) is a crucial molecule implicated in plastic modifications related to learning and memory. The expression of BDNF is highly regulated, which can lead to significant variability in BDNF levels in healthy subjects. Changes in BDNF expression might be associated with neuropsychiatric diseases, particularly in structures important for memory processes, including the hippocampus and parahippocampal areas. Curcumin is a natural polyphenolic compound that has great potential for the prevention and treatment of age-related disorders by regulating and activating the expression of neural protective proteins such as BDNF. This review discusses and analyzes the available scientific literature on the effects of curcumin on BDNF production and function in both in vitro and in vivo models of disease.

Hepatic benefits of sodium-glucose cotransporter 2 inhibitors in liver disorders.

Diabetic patients are at higher risk of liver dysfunction compared with the normal population. Thus, using hypoglycemic agents to improve liver efficiency is important in these patients. Sodium-glucose cotransporters-2 inhibitors (SGLT2i) are newly developed antidiabetic drugs with potent glucose-lowering effects. However, recent limited evidence suggests that they have extra-glycemic benefits and may be able to exert protective effects on the liver. Hence, these drugs could serve as promising pharmacological agents with multiple benefits against different hepatic disorders. In this review, the current knowledge about the possible effects of SGLT2 inhibitors on different forms of liver complications and possible underlying mechanisms are discussed.

Modulation of the ubiquitin-proteasome system by phytochemicals: Therapeutic implications in malignancies with an emphasis on brain tumors.

Regarding the multimechanistic nature of cancers, current chemo- or radiotherapies often fail to eradicate disease pathology, and frequent relapses or resistance to therapies occur. Brain malignancies, particularly glioblastomas, are difficult-to-treat cancers due to their highly malignant and multidimensional biology. Unfortunately, patients suffering from malignant tumors often experience poor prognoses and short survival periods. Thus far, significant efforts have been conducted to discover novel and more effective modalities. To that end, modulation of the ubiquitin-proteasome system (UPS) has attracted tremendous interest since it affects the homeostasis of proteins critically engaged in various cell functions, for example, cell metabolism, survival, proliferation, and differentiation. With their safe and multimodal actions, phytochemicals are among the promising therapeutic tools capable of turning the operation of various UPS elements. The present review, along with an updated outline of the role of UPS dysregulation in multiple cancers, provided a detailed discussion on the impact of phytochemicals on the UPS function in malignancies, especially brain tumors.

A review on the efficacy and safety of lipid-lowering drugs in neurodegenerative disease.

There is a train of thought that lipid therapies may delay or limit the impact of neuronal loss and poor patient outcomes of neurodegenerative diseases (NDDs). A variety of medicines including lipid lowering modifiers (LLMs) are prescribed in NDDs. This paper summarizes the findings of clinical and observational trials including systematic reviews and meta-analyses relating to LLM use in NDDs published in the last 15 years thus providing an up-to-date evidence pool. Three databases were searched PubMed, CINAHL, and Web of Science using key terms relating to the review question. The findings confirm the benefit of LLMs in hyperlipidemic patients with or without cardiovascular risk factors due to their pleotropic effects. In NDDs LLMs are proposed to delay disease onset and slow the rate of progression. Clinical observations show that LLMs protect neurons from α-synuclein, tau, and Aß toxicity, activation of inflammatory processes, and ultimately oxidative injury. Moreover, current meta-analyses and clinical trials indicated low rates of adverse events with LLMs when used as monotherapy. LLMs appear to have favorable safety and tolerability profiles with few patients stopping treatment due to severe adverse effects. Our collated evidence thus concludes that LLMs have a role in NDDs but further work is needed to understand the exact mechanism of action and reach more robust conclusions on where and when it is appropriate to use LLMs in NDDs in the clinic.

Association of C-reactive protein with histological, elastographic, and sonographic indices of non-alcoholic fatty liver disease in individuals with severe obesity.

BACKGROUND: Inflammation is critical in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). hs-CRP, an inflammatory marker, is considered one of the prognostic predictors of hepatic damage progression in NAFLD in some studies. METHODS: We assessed the concordance of hs-CRP concentrations and liver steatosis, steatohepatitis, and fibrosis based on elastography, sonography and liver biopsy findings in patients with severe obesity undergoing bariatric surgery. RESULTS: Among 90 patients, 56.7% showed steatohepatitis and 8.9% severe fibrosis. Hs-CRP were significantly associated with liver histology in an adjusted regression model (OR 1.155, 95% CI 1.029-1.297, p = 0.014; OR 1.155, 1.029-1.297, p = 0.014; OR 1.130, 1.017-1.257, p = 0.024 for steatosis, steatohepatitis, and fibrosis, respectively). The ROC curve, a cutoff of hs-CRP = 7 mg/L, showed a reasonable specificity (76%) for detecting biopsy-proven fibrosis and steatosis. CONCLUSION: hs-CRP was associated with any degree of histologically diagnosed liver damage, and it had a reasonable specificity for predicting biopsy-proven steatosis and fibrosis in obese individuals. Further studies are needed to identify non-invasive biomarkers that could predict NALFD progression due to the relevant health risks linked to liver fibrosis.

Evaluation of DNA methylation in BDNF, SLC6A4, NR3C1 and FKBP5 before and after treatment with selective serotonin-reuptake inhibitor in major depressive disorder.

Aim: To identify the DNA methylation status of related genes in major depressive disorder following selective serotonin-reuptake inhibitor treatment. Materials & methods: 45 patients with major depressive disorder and 45 healthy volunteers were considered experimental and control groups, respectively. High-resolution melting real-time PCR was implemented to evaluate DNA methylation. Results: After 100 days of selective serotonin-reuptake inhibitor treatment, methylation of promoter CpG sites of BDNF, NR3C1, FKBP5 and SLC6A4 was significantly reduced. Compared with before treatment, patients' Hamilton Depression Rating Scale scores were significantly reduced after selective serotonin-reuptake inhibitor treatment (p ≤ 0.0001). Conclusion: Based on the proven effect of antidepressants on DNA methylation and gene expression, these medications can improve the treatment process and reduce depression scores after treatment.

Effects of curcumin on low-density lipoprotein oxidation: From experimental studies to clinical practice.

Atherosclerosis is the most frequent cause of death globally. Oxidized low-density lipoprotein (ox-LDL) has an essential role in the formation of atherosclerotic plaques and foamy macrophages. Ox-LDL increases the uptake of cholesterol by macrophages and is the major cause of blood flow disruption. Ox-LDL is produced during oxidative stress and treatment with antioxidants could inhibit the production and function of ox-LDL. Curcumin is a potent antioxidant and has a strong track record in the treatment of numerous diseases. Recent studies indicate that Curcumin exerts a lipid-lowering effect, and can modulate the formation of atherosclerotic plaque. The current review focuses upon the role of Curcumin in oxidation of LDL and foam cell formation in atherosclerotic lesions.

Effect of Bariatric Surgery on Flow-Mediated Vasodilation as a Measure of Endothelial Function: A Systematic Review and Meta-Analysis.

Objectives. Flow mediated vasodilation (FMD) is a marker of endothelial function and its decline is related to increased cardiovascular risk. This systematic review and meta-analysis evaluated the impact of bariatric surgery on FMD. Materials and methods. A systematic literature search in PubMed, Scopus, Embase, and Web of Science was performed to 1 May 2021. Meta-analysis was performed using Comprehensive Meta-Analysis (CMA) V2 software. All types of bariatric surgery were considered, with the inclusion that FMD had to have been tested before and after the surgical procedure. Meta-analysis was carried out using a random-effects model and the generic inverse variance approach. The leave-one-out approach was used for sensitivity analysis. To assess metabolic parameter confounders, a weighted random-effects meta-regression was used. Results. A meta-analysis and a systematic review of 23 studies (n = 891 individuals) demonstrated improvement in FMD following bariatric surgery (weighted mean difference (WMD): 5.867, 95% CI: 4.481, 7.252, p < 0.001; I2: 96.70). Iteratively removing each item in the meta-analysis did not result in a significant alteration in the pooled estimate of effect size. There was an improvement in FMD for up to 6 months following bariatric surgery in a meta-analysis from 7 trials that included 356 subjects (WMD: 5.248, 95% CI: 2.361, 8.135, p < 0.001; I2: 98.18). The meta-analysis from 9 trials (n = 414 subjects) showed an improvement in FMD 6 to 12 months after bariatric surgery (WMD: 5.451, 95% CI: 3.316, 7.587, p < 0.001; I2: 94.18). The meta-analysis from 10 trials (n = 414 subjects) demonstrated an improvement in FMD 12 months after bariatric surgery (WMD: 2.401, 95% CI: 0.944, 3.859, p = 0.001; I2: 88.35). Random-effects meta-regression did not show any association between the alteration in FMD and percent body mass index (BMI) change (slope: 0.0258; 95% CI: −0.323, 0.375; p = 0.884), or changes in blood pressure; however, there was an association between the changes in FMD and the duration of follow-up (slope: −0.106; 95% CI: −0.205, −0.008; p = 0.033) with greater changes in FMD after 12 months. Conclusions. Bariatric surgery significantly improved FMD that increased with time, and the resultant improvement in endothelial function was independent of weight loss or a reduction in blood pressure.

Association between Oxidative Burden and Restenosis: A Case-Control Study.

Background: In-stent restenosis (ISR) is an important clinical complication that occurs following stent implantation. The application of drug-eluting stents (DES) and even consumption of drugs such as antiplatelet agents and statins are not completely effective in reducing ISR risk. Since the number of these patients continues to rise, it is pivotal to detect patients who are at a higher risk of ISR. In addition, identification of biochemical markers of ISR could give the right perspective on choosing the proper strategy to treat these patients. Several pathophysiological pathways including oxidative stress (OS) are implicated in the progression of ISR. Hence, this study aimed to evaluate the association between oxidative/anti-oxidative markers and ISR. Methods: This was a case-control study which comprised 21 ISR, 26 NISR (non-ISR), and 20 healthy subjects. The serum levels of OS markers including malondialdehyde (MDA), thiol groups (GSH), total antioxidant capacity (TAC), and the activity of serum antioxidant enzymes such as glutathione peroxidase (GPx) and superoxide dismutase (SOD) were assessed by colorimetric methods. The overall oxidative burden was assessed using a pro-oxidant-antioxidant balance (PAB) assay. Results: MDA levels were considerably higher in the ISR group when compared to healthy subjects (P = 0.004). PAB also indicated significantly higher values in both ISR (P < 0.001) and NISR (P < 0.001) groups related to healthy subjects. No significant differences were observed between the studied groups regarding thiol levels, antioxidant enzyme activities, and TAC. Multinomial logistic regression analysis showed that elevated serum levels of MDA (OR: 1.028, 95% CI: 1.008-1.048; P = 0.006) and PAB (OR: 1.076, 95% CI: 1.017-1.139; P = 0.011) were significantly associated with higher ISR risk; however, increased values of TAC (OR: 0.990, 95% CI: 0.982-0.999; P = 0.030) were significantly associated with decreased ISR risk, while after adjustment for confounders, only SOD activity (OR: 0.0, 95% CI: 0.0-0.0; P < 0.001) and PAB value (OR: 1.866, 95% CI: 1.856-1.900; P < 0.001) showed association with ISR risk. Conclusion: According to the present findings, some oxidative and antioxidative markers like PAB and SOD activity showed the potential in the prediction of ISR risk.

Evaluating the Effects of Curcumin on the Cytokine Storm in COVID-19 Using a Chip-Based Multiplex Analysis.

SARS-CoV-2 can stimulate the expression of various inflammatory cytokines and induce the cytokine storm in COVID-19 patients leading to multiple organ failure and death. Curcumin as a polyphenolic compound has been shown to have anti-inflammatory properties and inhibit the release of numerous pro-inflammatory cytokines. We present multiplex analysis using the Evidence Investigator biochip system to determine the effect of curcumin on serum level of cytokines which are typically elevated in cytokine storm events, including tumor necrosis factor (TNF-α), interleukin 6 (IL-6), and IL-10.

Liver Protective Effect of Fenofibrate in NASH/NAFLD Animal Models.

Nonalcoholic fatty liver disease (NAFLD) is initiated by excessive fat buildup in the liver, affecting around 35% of the world population. Various circumstances contribute to the initiation and progression of NAFLD, and it encompasses a wide range of disorders, from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and liver cancer. Although several treatments have been proposed, there is no definitive cure for NAFLD. In recent decades, several medications related to other metabolic disorders have been evaluated in preclinical studies and in clinical trials due to the correlation of NAFLD with other metabolic diseases. Fenofibrate is a fibrate drug approved for dyslipidemia that could be used for modulation of hepatic fat accumulation, targeting peroxisome proliferator-activator receptors, and de novo lipogenesis. This drug offers potential therapeutic efficacy for NAFLD due to its capacity to decrease the accumulation of hepatic lipids, as well as its antioxidant, anti-inflammatory, and antifibrotic properties. To better elucidate the pathophysiological processes underlying NAFLD, as well as to test therapeutic agents/interventions, experimental animal models have been extensively used. In this article, we first reviewed experimental animal models that have been used to evaluate the protective effects of fenofibrate on NAFLD/NASH. Next, we investigated the impact of fenofibrate on the hepatic microcirculation in NAFLD and then summarized the beneficial effects of fenofibrate, as compared to other drugs, for the treatment of NAFLD. Lastly, we discuss possible adverse side effects of fenofibrate on the liver.

The Predictive Role of Parathyroid Hormone for Nonalcoholic Fatty Liver Disease following Bariatric Surgery.

Background: Morbid obesity is frequently complicated by chronic liver diseases, including nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), and fibrosis. Parathyroid hormone (PTH) is found to be elevated in morbid obesity due to the defective hepatic metabolism of vitamin D. Bariatric surgery is performed to help patients with BMI>40 kg/m2 to effectively lose weight, particularly in patients with obesity who are afflicted with complications such as NAFLD/NASH. Objective: This study aimed to evaluate the PTH level as a predictor of hepatic function in individuals with morbid obesity who have undergone bariatric surgery. Methods: Ninety subjects with morbid obesity referred for Roux en-Y gastric bypass surgery were recruited. After IRB approval, demographic profiles, anthropometric factors, liver biopsy, and laboratory tests were obtained. The two-dimensional shear wave elastography (2D-SWE) technique was applied to assess hepatic stiffness. Results: A significant reduction occurred six months after bariatric surgery in the anthropometric indices (p < 0.001), hepatic elasticity (p=0.002), alanine aminotransferase (p < 0.001), serum alkaline phosphatase (p < 0.001), gamma-glutamyl transpeptidase (GGT) (p < 0.001), and nonalcoholic fatty liver disease fibrosis score (NFS) (p < 0.001). Serum PTH concentration was not predictive of postsurgical liver fibrosis and steatosis at six months but could predict weight loss success rate. No significant alteration in serum PTH levels was observed between presurgical vs. postsurgical time points. Conclusion: A significant reduction was observed in the anthropometric parameters, liver enzymes, and hepatic elasticity after bariatric surgery. No significant effect was found on PTH levels.

Protective Effect of Cinnamaldehyde on METH-induced Neurotoxicity in PC12 Cells via Inhibition of Apoptotic Response and Oxidative Stress.

Methamphetamine (METH) is a potent central nervous system (CNS) stimulant and frequently used illegal drugs. Repeated exposure to METH can induce degenerative changes in dopaminergic and serotonergic axons. There is no standard medical treatment for METH's neurotoxic effects. Cinnamaldehyde is an important compound of cinnamon and has activities against neurological disorders. The present study was designed to examine the neuroprotective effect of trans-cinnamaldehyde (TCA) on METH-induced cytotoxicity. PC12 cells were treated with METH (2.5 mM) 24 h after treated with different concentrations of TCA (3.75- 50 µM). The percentage of cell survival was evaluated by MTT assay and the following parameters were measured to detect apoptosis and oxidative stress responses: DNA fragmentation, ROS production and GSH content. Exposure to 2.5 mM METH decreased the cell viability and GSH levels, caused the generation of reactive oxygen species and ultimately induced apoptosis. Pretreatment with TCA at 3.125-25 µM significantly attenuated cell viability loss. TCA, especially at a concentration of 12.5 and 25 µM, decreased the apoptosis and ROS generation and increased the GSH level compared with the METH group. The findings of the present study suggested that TCA exerted a protective effect against METH-induced neurotoxicity through mechanisms related to antioxidant and anti-apoptosis. It is suggested that TCA may be useful for the prevention and treatment of harmful effects of METH on the brain.

Investigation of the Effects of Difluorinated Curcumin on Glycemic Indices in Streptozotocin-Induced Diabetic Rats.

BACKGROUND: Curcumin is an antioxidant agent that improves glycemia in animal models of diabetes. Clinically curcumin use is limited due to poor solubility, weak absorption, and low bioavailability; therefore, this study to investigate the effects of curcumin's analog, difluorinated curcumin (CDF), on fasting blood glucose (FBG), oral glucose tolerance test (OGTT), and insulin tolerance test (ITT), in streptozotocin (STZ)-induced diabetic rats was undertaken. METHODS: STZ-induced diabetes rats were randomly assigned to six groups (7 rats per group). They were treated daily by oral gavage with curcumin (200 and 100 mg/kg/day), CDF (200 and 100 mg/kg/day), and metformin (200 mg/kg/day) as a positive control group, for 4 weeks. Two diabetic control (DC) and normal control (NC) groups (non-diabetic rats) received normal saline and citrate buffer, respectively. FBG was measured at the beginning and end of the treatment (Day 0 and week 4) and OGTT and ITT were performed to determine glucose tolerance and insulin sensitivity. RESULTS: Cur100, CDF 100, and CDF200 significantly decreased FBG levels after 4 weeks oral administration by -34% (-150 mg/dL ± 70, p = 0.02), -36% (123 mg/dL ±67, p < 0.04), and - 40% (-189 mg/dL ± 91, p = 0.03), respectively. Glucose sensitivity by OGTT showed a significant improvement in glucose tolerance ability in all treated groups compared with DC group. ITT demonstrated that insulin response improved significantly in Cur100 and CDF 200 groups. CONCLUSION: Overall, CDF improved glucose tolerance and insulin sensitivity, while reducing FBG compared to curcumin, suggesting that curcumin analogs may have therapeutic utility in diabetes.

The Effects of Curcumin on the Side Effects of Anticancer Drugs in Chemotherapy: A Randomized Controlled Trial.

Curcumin, the active ingredient of the spice turmeric, has been shown to have anticancer activities in several preclinical and clinical studies. The prophylactic effect of curcumin against chemotherapy-induced damage and side effects was evaluated in a double-blind, placebo-controlled randomized trial. Eighty cancer patients on standard chemotherapy regimens were randomly assigned to receive curcumin as adjuvant therapy (500 mg per 12 hours) and matched control group to receive placebo for 9 weeks. Pre- and post-intervention, the changes in the health-related quality-of-Life (QoL) score (based on the University of Washington Quality-of-Life (UW-QoL) questionnaire, version 3), clinical symptoms, and hematological and biochemical parameters were assessed. Comparison between groups based on total QoL score showed that curcumin supplementation was not associated with improved QoL (P = 0.102). Hematological and biochemical analysis showed no statistical differences between the groups at the end of the trial (P > 0.05). However, during the trial, significant differences were observed in hemoglobin (Hb), hematocrit (HCT), lactic acid dehydrogenase (LDH), serum glutamic-oxaloacetic transaminase (SGOT), and anaplastic lymphoma kinase (ALK) between the groups (P < 0.05). Future studies in a larger homogenous population of cancer patients are required to confirm the adjuvant effect of curcumin on chemotherapy-induced QoL.

Antioxidant Effects of Trehalose in an Experimental Model of Type 2 Diabetes.

BACKGROUND: Oxidative stress that occurs as a consequence of the imbalance between antioxidant activity and free radicals can contribute in the pathogenesis of metabolic disorders, such as type 2 diabetes mellitus (T2DM). Antioxidant therapies have been proposed as possible approaches to treat and attenuate diabetic complications. The purpose of this study was to evaluate potential antioxidant effects of trehalose on oxidative indices in a streptozotocin (STZ)-induced diabetic rat model. METHODS: Diabetic rats were divided randomly into five treatment groups (six rats per group). One test group received 45 mg/kg/day trehalose via intraperitoneal injection, and another received 1.5 mg/kg/day trehalose via oral gavage for 4 weeks. Three control groups were also tested including nondiabetic rats as a normal control (NC), a nontreated diabetic control (DC), and a positive control given 200 mg/kg/day metformin. Levels of thiol groups (-SH), and serum total antioxidant capacity were measured between control and test groups. In addition, superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities were assessed. RESULTS: In both oral and injection trehalose-treated groups, a marked increase was observed in serum total antioxidant capacity (TAC) (p > 0.05) and thiol groups (-SH) (p < 0.05). Also, SOD and GPx activities were increased after 4 weeks of treatment with trehalose. CONCLUSION: In conclusion, the present results indicate ameliorative effects of trehalose on oxidative stress, with increase antioxidant enzyme activities in STZ-induced diabetic rats.

Boosting GLP-1 by Natural Products.

The prevalence of diabetes mellitus is growing rapidly. Diabetes is the underlying cause of many metabolic and tissue dysfunctions, and, therefore, many therapeutic agents have been developed to regulate the glycemic profile. Glucagon-like peptide-1 (GLP-1) receptor agonists are a newly developed class of antidiabetic drugs that have potent hypoglycemic effects via several molecular pathways. In addition to synthetic GLP-1 receptor agonists, some evidence suggests that natural products may have modulatory effects on GLP-1 expression and secretion. In the current study, we conclude that certain herbal-based constituents, such as berberine, tea, curcumin, cinnamon, wheat, soybean, resveratrol, and gardenia, can exert an influence on GLP-1 release.

Counteracting arsenic toxicity: Curcumin to the rescue?

Arsenicosis leads to various irreversible damages in several organs and is considered to be a carcinogen. The effects of chronic arsenic poisoning are a result of an imbalance between pro- and antioxidant homeostasis, oxidative stress, as well as DNA and protein damage. Curcumin, the polyphenolic pigment extracted from the rhizome of Curcuma longa, is well-known for its pleiotropic medicinal effects. Curcumin has been shown to have ameliorative effects in arsenic-induced genotoxicity, nephrotoxicity, hepatotoxicity, angiogenesis, skin diseases, reproductive toxicity, neurotoxicity, and immunotoxicity. This review aims to summarize the scientific evidence on arsenic toxicity in various organs and the ameliorative effects of curcumin on the arsenic toxicity.