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Purpose To investigate the phytochemical uptake following human consumption of Montmorency tart cherry (L. Prunus cerasus) and influence of selected phenolic acids on vascular smooth muscle cells in vitro. Methods In a randomised, double-blinded, crossover design, 12 healthy males consumed either 30 or 60 mL of Montmorency tart cherry concentrate. Following analysis of the juice composition, venous blood samples were taken before and 1, 2, 3, 5 and 8 h post-consumption of the beverage. In addition to examining some aspects of the concentrate contents, plasma concentrations of protocatechuic acid (PCA), vanillic acid (VA) and chlorogenic (CHL) acid were analysed by reversed-phase high-performance liquid chromatography (HPLC) with diode array for quantitation and mass spectrometry detection (LCMS) for qualitative purposes. Vascular smooth muscle cell migration and proliferation were also assessed in vitro. Results Both the 30 and 60 mL doses of Montmorency cherry concentrate contained high amounts of total phenolics (71.37 ± 0.11; 142.73 ± 0.22 mg/L) and total anthocyanins (62.47 ± 0.31; 31.24 ± 0.16 mg/L), as well as large quantities of CHL (0.205 ± 0.24; 0.410 ± 0.48 mg/L) and VA (0.253 ± 0.84; 0.506 ± 1.68 mg/L). HPLC/LCMS identified two dihydroxybenzoic acids (PCA and VA) in plasma following MC concentrate consumption. Both compounds were most abundant 1–2 h post-initial ingestion with traces detectable at 8 h post-ingestion. Cell migration was significantly influenced by the combination of PCA and VA, but not in isolation. There was no effect of the compounds on cell proliferation. Conclusions These data show new information that phenolic compounds thought to exert vasoactive properties are bioavailable in vivo following MC consumption and subsequently can influence cell behaviour. These data may be useful for the design and interpretation of intervention studies investigating the health effects of Montmorency cherries

Background Typhae Pollen (TP) and Trogopterus Feces (TF) are well-known traditional medicine in china which widely used for thousands of years as drug pair called Shixiao San for treatment of blood stasis syndrome, specially shown great efficacy in gynecological disease. Typhaneoside, vanillic acid and p -coumaric acid are the main bioactive components of Typhae Pollen. This study was carried out for comparing the pharmacokinetic profile of these three major bioactive components in rats after oral administration of Typhae Pollen-Trogopterus Feces (TP-TF) drug pair before and after compatibility. Methods A sensitive and rapid UPLC-TQ/MS method has been developed for simultaneous quantification of the three main bioactive compounds in blood at different time points after oral administration of Typhae Pollen (TP) and the combination with Trogopterus Feces (TF). Results There were significant differences of C max , T max , T 1/2 and AUC 0~t for three bioactive compounds among the groups, for typhaneoside with the most highest plasma concentration of 370.86 ± 315.71 ng/mL and more longer T max in TP-TF co-decoction group (C M ); for vanillic acid, TP-TF co-decoction group (C M ) had a good absorption with C max (3870.99 ± 2527.99 ng/mL) and T max (1.47 ± 3.20 h); for p -coumaric acid, it had similar pharmacokinetic characteristics with vanillic acid. Conclusions The three bioactive components in Typhae Pollen (TP) were simultaneously determined by UPLC-TQ/MS and had a good absorption in rat plasma after the combination with Trogopterus Feces (TF).

This study aimed to evaluate the cancer chemopreventive activity of vanillic acid (VA) in diethylnitrosamine- and 1,2-dimethylhydrazine-induced liver and colon carcinogenesis in rats. VA did not induce the formation of hepatic glutathione S-transferase placental form (GST-P) positive foci and colonic aberrant crypt foci, demonstrating no carcinogenic activity. VA (75 mg kg−1 body weight) could significantly reduce the number and areas of hepatic GST-P positive foci when administered before carcinogen injections, but no such effect was seen when it was administered after carcinogen injection. No protection was seen in the colon when VA was treated before or after carcinogen injection. Immunohistochemical studies demonstrated the decreased expression of proliferating cell nuclear antigen and the induction of apoptosis. Mechanistic studies showed that VA significantly induced the expression of GSTA-5 and Nrf-2 genes, which are associated with the detoxification system. Likewise, the antiproliferative effect was noticed by the reduction of Cyclin D1 expression. The apoptotic activity may be due to the upregulation of Caspase-3 and Bad levels and downregulation of the Bcl-2 level. These data suggest that VA exhibited significant protection against diethylnitrosamine- and 1,2-dimethylhydrazine-induced hepatocarcinogenesis, which might be related to the induction of the detoxifying enzyme, the reduction of proliferation and the induction of apoptosis.

Vanillic acid is a phenolic compound recognized for its use as a flavoring agent in the food industry. It can be found in a variety of products, such as thyme, rice, oranges, cherries, green tea, wine, and beer. Vanillic acid has been substantiated to show various beneficial pharmacological properties including anti-inflammatory, antibacterial, cardioprotective, hepatoprotective, antitumorigenic, free radical scavenging, antioxidant and even antivenomous activity. Since vanillic acid has low bioavailability, and bioavailability of a compound depends (among other factors) on its chemical structure, testing isomers of vanillic acid may yield promising results. Several structural and biological studies were carried out to determine the correlation between the molecular structure and biological activity of vanillic acid and its isomers (isovanillic acid and o -vanillic acid). Studies have shown that changes in the electronic structure of vanillic acids affect their different reactivity, antioxidant activity, and cytotoxicity. O -vanillic acid, characterized by the highest reactivity, is a weak antioxidant and the best cytotoxic compound. No direct correlation was observed between the antioxidant activity of vanillic acids and their toxic effect on model cell lines, probably due to the different mechanisms of action in the phenomena studied.

Methotrexate-induced nephrotoxicity is a medical emergency which is associated with a variety of side effects. Vanillic acid (VA), as an antioxidant, removes free radical oxygen to protect cell defense. Therefore, this study investigated VA’s beneficial effects on nephrotoxicity induced by methotrexate through its anti-apoptosis, antioxidant, and anti-inflammatory properties. Our study included five groups of male Wistar rats (n = 8): sham, MTX (Methotrexate) group: rats receiving methotrexate (20 mg/kg, intraperitoneally) on Day 2. Moreover, the remaining groups consisted of animals that received vanillic acid (25, 50, and 100 mg/kg, orally for seven days) plus MTX on the 2 nd day. The rats were deeply anesthetized on the eighth day to obtain blood and renal tissue samples. The results showed that MTX can increase blood urea nitrogen and creatinine. However, VA (50 and 100 mg/kg) improved renal function as approved by histological findings. Compared with MTX-treated rats, VA enhanced the contents of total antioxidant capacity (TAC) and reduced renal malondialdehyde (MDA). Moreover, VA reduced mRNA expressions of caspase-3 and Bcl-2-associated x protein (Bax) and caused mRNA overexpression of the renal B-cell lymphoma-2 (Bcl-2), and Nrf-2 (Nuclear factor erythroid 2-related factor 2) compared to the MTX group. Also, VA administration significantly reduced inflammatory agents. Overall, VA protects the kidneys against methotrexate-induced nephrotoxicity via anti-apoptosis, antioxidant, and anti-inflammatory properties. Our results revealed that the most effective dose of VA was 100 mg/kg.

Particulate matter (PM) inhalation is an established trigger of cardiovascular events such as cardiac arrhythmias that occur within hours to days after exposure. Higher daily PM levels are related to acute increases in systemic arterial blood pressure (BP). The aim of the present study was to evaluate the effects of PM 10 on electrocardiogram (ECG) parameters, blood pressure, lipid peroxidation (MDA), xanthine oxidase, and antioxidant enzyme in healthy rats and also to examine the protective effects of vanillic acid (VA) in this respect. Eighty male Wistar rats were divided into eight groups ( n  = 10), namely control (normal saline, gavage), VAc (10 mg/kg), sham (normal saline, intratracheal instillation), VA (10 mg/kg VA, 10 days gavage +0.1 ml normal saline, intratracheal instillation), PM1 (0.5 mg/kg), PM2 (2.5 mg/kg), PM3 (5 mg/kg), PM3 + VA (5 mg/kg, intratracheal instillation + 10 mg/kg VA, 10 days, gavage) groups. The rats were anesthetized and 0.1 ml of saline as well as a certain concentration of PM 10 was instilled into the trachea and it was repeated after 48 h, then 30 min after that, PR interval, QTc, and systolic blood pressure were measured. The activities of antioxidant enzymes, xanthine oxidase (XOX), and malondialdehyde (MDA) were measured in plasma by special Kits. A significant increase in blood pressure (BP), PR interval, QTc, MDA, and XOX and a significant decrease in antioxidant enzyme (CAT, SOD, and GPx) occurred in PM 10 groups. Vanillic acid ameliorated blood pressure, QTc, PR interval, XOX, MDA, and increased antioxidant enzymes (SOD, CAT, and GPx) significantly. In the present study, it was shown that PM 10 had devastating effects on the heart and blood pressure, probably due to the increased oxidative stress in healthy rats. Vanillic acid could improve the symptoms of PM 10 exposure and can be used as an antioxidant agent against the harmful effects of PM 10 .

To evaluate dose‐dependent cytotoxicity effects of indoor dust particles (DPs) collected from Neyshabur, Iran, in vitro on A545 cells and in vivo on lungs of healthy male Wistar rats, as well as the antioxidant effects of vanillic acid (VA) against DP inhalation. Heavy metal levels in DPs collected from high‐traffic (HT), medium‐traffic, low‐traffic or rural (LT) zones were measured, and their cytotoxicity effects were evaluated by MTT assay. In vivo evaluations were conducted after rats were exposed to DPs collected from HT or LT in the presence or absence of VA. Exposure to DPs increased the activity of serum superoxide dismutase; the serum level of malondialdehyde; and mRNA expression of TNFα, IL6, CXCL15 and CYP1A1 in the lung homogenate groups receiving HT and LT compared to the control group. DP effects in the groups receiving HT were higher than those of LT. Concomitant VA intake attenuated the adverse effects mediated by DPs in the HT and LT groups. DPs had adverse effects on the lungs of healthy rats, probably because of the accumulated oxidative stress agents. VA could ameliorate the effects of DPs and may be considered as a protective substance against the undesirable effects of DPs.

Background There is growing evidence that platelet‐related parameters can influence a wide range of cardiovascular diseases. However, the effect of platelet‐related parameters on cardiac hypertrophy is unknown. To verify this, the present study proposes to use Mendelian randomization (MR) to explore bidirectional causality between multiple platelet‐related parameters and cardiac hypertrophy and to assess the potential mediating role of plasma metabolites. Methods Single‐nucleotide polymorphisms (SNPs), the instrumental variable required for the study, were obtained through the public genome‐wide association study (GWAS) database, and samples were obtained from European populations. We obtained summary statistics of cardiac hypertrophy (4113 cases, 839,403 controls) after GWAS meta‐analysis of two independent datasets. In this study, we mainly used the inverse variance weighted (IVW) method to assess the causal effect; two‐step MR analysis was used to assess the mediating effect. Results MR analysis showed a positive causal relationship between mean platelet volume (MPV) and the risk of cardiac hypertrophy (odds ratio, 1.72 for cardiac hypertrophy per one‐standard‐deviation increment in MPV; 95% confidence interval, 1.24 to 2.38; p = 0.001). Multivariate MR showed that the risk role of MPV in promoting cardiac hypertrophy persisted after adjustment for other platelet parameters. Mediation analysis via two‐step MR showed that this effect was partially mediated by vanillic acid glycine levels, with a mediation ratio of 20.4% (95% confidence interval, 3.7% to 40.7%). Conclusions This study revealed a positive causal relationship between MPV and cardiac hypertrophy risk, partly mediated by plasma vanillic acid glycine levels.

Excess free fatty acid accumulation from abnormal lipid metabolism results in the insulin resistance in peripheral cells, subsequently causing hyperinsulinemia, hyperglycemia and/or hyperlipidemia in diabetes mellitus (DM) patients. Herein, we investigated the effect of phenolic acids on glucose uptake in an insulin-resistant cell-culture model and on hepatic insulin resistance and inflammation in rats fed a high-fat diet (HFD). The results show that vanillic acid (VA) demonstrated the highest glucose uptake ability among all tested phenolic acids in insulin-resistant FL83B mouse hepatocytes. Furthermore, rats fed HFD for 16 weeks were orally administered with VA daily (30 mg/kg body weight) at weeks 13–16. The results show that levels of serum insulin, glucose, triglyceride, and free fatty acid were significantly decreased in VA-treated HFD rats (p < 0.05), indicating the protective effects of VA against hyperinsulinemia, hyperglycemia and hyperlipidemia in HFD rats. Moreover, VA significantly reduced values of area under the curve for glucose (AUCglucose) in oral glucose tolerance test and homeostasis model assessment-insulin resistance (HOMA-IR) index, suggesting the improving effect on glucose tolerance and insulin resistance in HFD rats. The Western blot analysis revealed that VA significantly up-regulated expression of hepatic insulin-signaling and lipid metabolism-related protein, including insulin receptor, phosphatidylinositol-3 kinase, glucose transporter 2, and phosphorylated acetyl CoA carboxylase in HFD rats. VA also significantly down-regulated hepatic inflammation-related proteins, including cyclooxygenase-2 and monocyte chemoattractant protein-1 expressions in HFD rats. These results indicate that VA might ameliorate insulin resistance via improving hepatic insulin signaling and alleviating inflammation pathways in HFD rats. These findings also suggest the potential of VA in preventing the progression of DM.

An investigation was made to reveal the protective effects of veratric acid (VA), a phenolic acid against atherogenic diet-induced hyperlipidemic rats. Male albino Wistar rats were fed with atherogenic diet (4% cholesterol, 1% cholic acid, and 0.5% 2-thiouracil) daily for 30 days and treated with VA (40 mg/kg body weight) daily for a period of 30 days. Rats fed with atherogenic diet showed significant ( P  < 0.05) elevation in the level of plasma lipids, systolic and diastolic blood pressure, oxidative stress markers (thiobarbituric acid reactive substances, lipid peroxides) and significant ( P  < 0.05) reduction in the activities of enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic (vitamin C, vitamin E, and reduced glutathione) antioxidants in erythrocytes, plasma, and tissues (liver, kidney, and aorta). Oral administration of VA (40 mg/kg body weight) for 30 days to atherogenic diet fed rats markedly attenuates systolic, diastolic blood pressure and lipid peroxidation products. Further, VA treatment significantly improved enzymatic and non-enzymatic antioxidants levels and showed beneficial effects on lipid profile in atherogenic diet rats. All the above alterations were supported by histopathological observations. These results indicate that oral administration of VA ameliorates atherogenic diet-induced hyperlipidemia in rats by its free radical scavenging; improving the antioxidants and lipid lowering properties.