Yi-Shuai Zhang

Alpha lipoic acid protects heart against myocardial ischemia-reperfusion injury through a mechanism involving aldehyde dehydrogenase 2 activation

Recent studies demonstrate that alpha lipoic acid can prevent nitroglycerin tolerance by restoring aldehyde dehydrogenase 2 (ALDH2) activity and ALDH2-mediated detoxification of aldehydes is thought as an endogenous mechanism against ischemia-reperfusion injury. This study was performed to explore whether the cardioprotective effect of alpha lipoic acid was related to activation of ALDH2 and the underlying mechanisms. In a Langendorff model of ischemia-reperfusion in rats, cardiac function, activities of creatine kinase (CK) and ALDH2, contents of 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) were measured. In a cell model of hypoxia-reoxygenation, the apoptosis, ALDH activity, reactive oxygen species level, 4-HNE and MDA contents were examined. In the isolated hearts, ischemia-reperfusion treatment led to cardiac dysfunction accompanied by an increase in 4-HNE and MDA contents. Pretreatment with lipoic acid significantly up-regulated myocardial ALDH2 activity concomitantly with an improvement of cardiac dysfunction and a decrease in 4-HNE and MDA contents, these effects were blocked by the inhibitor of ALDH2. Similarly, in the cultured cardiomyocytes, hypoxia-reoxygenation treatment induced apoptosis accompanied by an increase in the production of reactive oxygen species, 4-HNE and MDA. Administration of lipoic acid significantly up-regulated cellular ALDH2 activity concomitantly with a reduction in apoptosis, production of reactive oxygen species, 4-HNE and MDA, these effects were reversed in the presence of ALDH2 or PKCε inhibitors. Our results suggest that the cardioprotective effects of lipoic acid on ischemia-reperfusion injury are through a mechanism involving ALDH2 activation. The regulatory effect of lipoic acid on ALDH2 activity is dependent on PKCε signaling pathway.

Calcitonin gene-related peptide-mediated antihypertensive and anti-platelet effects by rutaecarpine in spontaneously hypertensive rats.

We have previously reported that Chinese traditional medicine rutaecarpine (Rut) produced a sustained hypotensive effect in phenol-induced and two-kidney, one-clip hypertensive rats. The aims of this study are to determine whether Rut could exert antihypertensive and anti-platelet effects in spontaneously hypertensive rats (SHR) and the underlying mechanisms. In vivo, SHR were given Rut and the blood pressure was monitored. Blood was collected for the measurements of calcitonin gene-related peptide (CGRP), tissue factor (TF) concentration and activity, and platelet aggregation, and the dorsal root ganglia were saved for examining CGRP expression. In vitro, the effects of Rut and CGRP on platelet aggregation were measured, and the effect of CGRP on platelet-derived TF release was also determined. Rut exerted a sustained hypotensive effect in SHR concomitantly with the increased synthesis and release of CGRP. The treatment of Rut also showed an inhibitory effect on platelet aggregation concomitantly with the decreased TF activity and TF antigen level in plasma. Study in vitro showed an inhibitory effect of Rut on platelet aggregation in the presence of thoracic aorta, which was abolished by capsazepine or CGRP(8-37), an antagonist of vanilloid receptor or CGRP receptor. Exogenous CGRP was able to inhibit both platelet aggregation and the release of platelet-derived TF, which were abolished by CGRP(8-37). The results suggest that Rut exerts both antihypertensive and anti-platelet effects through stimulating the synthesis and release of CGRP in SHR, and CGRP-mediated anti-platelet effect is related to inhibiting the release of platelet-derived TF.

Preheating and roasting characteristics of hematite–magnetite (H–M) concentrate pellets

Abstract Regressive orthogonal design experiments have been carried out based on the analysis of the oxidation and induration behaviours of individual magnetite and hematite pellets. The research shows that the optimal pellet preheating time and temperature, and roasting time and temperature change with hematite/magnetite (H/M) ratio. Under the conditions of preheating temperature 900°C, preheating time 10 min, roasting temperature 1275°C and roasting time 15 min, the compression strength of preheated and roasted pellets is found to be respectively more than 444 N/pellet (N/P) and 3993 N/P when the magnetite content in the pellets exceeds 20%. The pellet strengths meet the requirements of rotary kilns and blast furnaces respectively.

Vanillyl nonanoate protects rat gastric mucosa from ethanol-induced injury through a mechanism involving calcitonin gene-related peptide

Previous studies have demonstrated that capsaicin-sensitive sensory nerves are involved in the protection of gastric mucosa against damage by various stimuli and calcitoin gene-related peptide (CGRP) is a potential mediator in this process. This study was performed to explore the effect of vanillyl nonanoate, a capsaicin analog, on ethanol-induced gastric mucosal injury and the possible underlying mechanisms. A rat model of gastric mucosal injury was induced by oral administration of acidified ethanol and gastric tissues were collected for analysis of gastric ulcer index, cellular apoptosis, the activities of caspase-3, catalase and superoxide dismutase (SOD), levels of CGRP, TNF-α and malondialdehyde (MDA). The results showed that acute administration of ethanol significantly increased gastric ulcer index concomitantly with increased cellular apoptosis, caspase-3 activity, TNF-α and MDA levels as well as decreased activities of catalase and SOD. Pretreatment with 1mg/kg vanillyl nonanoate significantly attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by increase of CGRP expression, and SOD activity and decrease of caspase-3 activity, TNF-α and MDA levels. The effects of vanillyl nonanoate were inhibited by capsazepine, an antagonist of capsaicin receptor. Our results suggested that vanillyl nonanoate was able to protect the gastric mucosa against ethanol-induced gastric mucosal injury. The underlying mechanism is related to stimulation of CGRP release and subsequent suppression of ethanol-induced inflammatory reaction, cellular apoptosis and oxidative stress.

Beneficial effects of capsiate on ethanol-induced mucosal injury in rats are related to stimulation of calcitonin gene-related Peptide release.

Capsiate is a non-pungent analogue of capsaicin from CH-19 Sweet peppers. Capsaicin is reported to trigger calcitonin gene-related peptide (CGRP) release through activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) and produces beneficial effects on gastric mucosa. This study aimed to investigate whether capsiate is able to produce beneficial effects on gastric mucosa and whether the protective effects of capsipate occur through a mechanism involving the activation of TRPV1 and CGRP release. A rat model of gastric mucosal injury was established by the oral administration of acidified ethanol. Gastric tissues were collected for analysis of the gastric ulcer index, cellular apoptosis, activities of caspase-3, catalase and superoxide dismutase (SOD), and levels of CGRP, TNF-α, and malondialdehyde (MDA). Our results show that the acute administration of ethanol significantly increased the gastric ulcer index concomitantly with an increase in cellular apoptosis, caspase-3 activity, and TNF-α and MDA levels, as well as a decrease in the activities of catalase and SOD. Pretreatment with 1 mg/kg capsiate attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by an increase in CGRP level, catalase, and SOD activities, and a decrease in caspase-3 activity, and TNF-α and MDA levels. The effects of capsiate were inhibited by capsazepine, an antagonist of TRPV1. These results suggest that capsiate is able to produce beneficial effects on ethanol-induced gastric mucosal injury. These effects are related to the stimulation of CGRP release through the activation of TRPV1.

Phloroglucinol protects gastric mucosa against ethanol-induced injury through regulating myeloperoxidase and catalase activities

It has been shown that oxidative stress plays an important role in the pathogenesis of ethanol‐induced acute gastric mucosal injury, and phloroglucinol, a smooth muscle relaxant, has been reported to possess anti‐oxidative properties. In this study, we explored the effect of phloroglucinol on ethanol‐induced gastric mucosal injury and the possible underlying mechanisms. The rat model of gastric mucosal injury was induced by oral administration of acidified ethanol, and the gastric tissues were collected for analysis of gastric ulcer index (UI), cellular apoptosis, anti‐O2˙ or OH˙ formation activity, malondialdehyde (MDA) content, and the activities of myeloperoxidase (MPO), catalase and glutathione peroxidase. The results showed that acute administration of ethanol significantly increased gastric UI concomitantly with the increased cellular apoptosis, MDA contents, MPO activity as well as the decreased activities of catalase and anti‐O2˙ or OH˙ formation, which was reversed by pretreatment with phloroglucinol. Although ethanol treatment significantly decreased the activity of glutathione peroxidase, pretreatment with phloroglucinol did not significantly affect the activity of the same. The results suggest that phloroglucinol could protect the gastric mucosa against ethanol‐induced injury, which is related to inhibiting the MPO activity and increasing the catalase activity in the gastric tissues.

Detailed Adsorption Studies of Active Humic Acid Fraction of a New Binder on Iron Ore Particles

Humic acid (HA) is used as one of organic active fractions of a new binder in the process of iron ore agglomeration. The purpose of this study was to determine the detailed adsorption characteristics of HA onto iron ore particles. The results demonstrated that the adsorption of HA was strongly dependent on solution pH, concentration, contact time and temperature. The chemical adsorption controlled the adsorption process of HA onto iron ore particles as typically found in earlier reported results. The adsorption kinetics of HA onto iron ore particles at different testing conditions was well described by the first-order model, which indicated that the adsorption rate is proportional to the concentration of HA. The adsorption isotherms of HA were determined by the fittings of the experimental data to two well-known isotherm models involving models: Langmuir and Freundlich. The Freundlich model (R-square > 0.97) appeared to fit the adsorption better than the Langmuir adsorption model, which indicated that multilayer absorption dominates the reaction of HA with iron ore particles. The value of exponent n (n > 1.0) for the Freundlich model indicated that the multilayer absorption of HA was hampered because of the appearance of the adsorbed HA on iron ore particles. These findings are useful for evaluating the adsorption capacity of MHA binder.

Protective effect of phloroglucinol against myocardial ischaemia-reperfusion injury is related to inhibition of myeloperoxidase activity and inflammatory cell infiltration.

1. It has been shown that phloroglucinol has anti‐inflammatory and anti‐oxidant properties. Both inflammatory cell infiltration and myeloperoxidase (MPO) activation play an important role in myocardial reperfusion injury. The aim of the present study was to explore the effect of phloroglucinol on myocardial reperfusion injury and the mechanisms involved.

Inhibition of vascular peroxidase alleviates cardiac dysfunction and apoptosis induced by ischemia–reperfusion

Myeloperoxidase (MPO) is involved in myocardial ischemia-reperfusion (IR) injury and vascular peroxidase (VPO) is a newly identified isoform of MPO. This study was conducted to explore whether VPO is involved in IR-induced cardiac dysfunction and apoptosis. In a rat Langendorff model of myocardial IR, the cardiac function parameters (left ventricular pressure and the maximum derivatives of left ventricular pressure and coronary flow), creatine kinase (CK) activity, apoptosis, VPO1 activity were measured. In a cell (rat-heart-derived H9c2 cells) model of hypoxia-reoxygenation (HR), apoptosis, VPO activity, and VPO1 mRNA expression were examined. In isolated heart, IR caused a marked decrease in cardiac function and a significant increase in apoptosis, CK, and VPO activity. These effects were attenuated by pharmacologic inhibition of VPO. In vitro, pharmacologic inhibition of VPO activity or silencing of VPO1 expression significantly suppressed HR-induced cellular apoptosis. Our results suggest that increased VPO activity contributes to IR-induced cardiac dysfunction and inhibition of VPO activity may have the potential clinical value in protecting the myocardium against IR injury.

Oxidising roasting behaviours of anthracite containing haematite pellets

Abstract In this investigation, the roasting features of haematite pellets to which a small amount of anthracite was added and the effects of carbon on the induration behaviours of the pellets were studied. The results indicate that the suitable dosage of pulverised anthracite is 1·0–1·5%. During the roasting, part of the original haematite grains in the pellets are reduced to magnetite, and some original haematite grains are decomposed into magnetite. Then, the newborn magnetite is oxidised to secondary haematite, which is beneficial to the recrystallisation of Fe2O3 in the fired pellets. Therefore, adding a certain proportion of anthracite is an effective way to improve the roasting strength of haematite pellets, as well as to reduce the roasting temperature and the total energy consumption of the pellet production.