Allicin Group Research Articles

Allicin as add-on therapy for Helicobacter pylori infection: A systematic review and meta-analysis.

BACKGROUNDAllicin (2-propene-1-sulfinothioic acid S-2-propenyl ester, diallyl thiosulfinate) extracted from garlic, has proven activity against Helicobacter pylori (H. Pylori) infection. In recent years, clinical trials have explored its utility as an add-on therapy with variable outcomes reported.AIMTo perform a systemic review of allicin as an add-on treatment for H. Pylori infection and assess its efficacy in randomized controlled trials (RCTs).METHODSElectronic databases including MEDLINE, EMBASE, the Web of Science, the Cochrane Database, the China National Knowledge Infrastructure Database, Chinese VIP Information Databases, Chinese Medical Databases, and the Wan-Fang Database were searched for keywords including “allicin”, “Helicobacter pylori”, “randomized clinical trials”, and their synonyms. A meta-analysis was performed using the fixed-effects model for low heterogeneity and the random-effects model for high heterogeneity with sensitivity analysis. Bias was evaluated using Egger’s tests. Trial sequential analysis (TSA) was used to evaluate information size and treatment benefits. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) was used to assess the level of quality, and studies were classed as “high quality”, “moderate quality”, “low quality”, and “very low quality”.RESULTSA total of eight RCTs consisting of 867 participants (435 from the allicin group and 432 from the control group) were included. Eradication rate in the allicin group (93.33%, 406/435) was significantly higher than that of the control group (83.56%, 361/432) [I2 = 0%, odds ratio (OR) = 2.75, 95% confidence interval (CI): 1.74-4.35, P < 0.001]. The healing rate of ulcers following H. pylori therapy in the allicin group (86.17%, 349/405) was significantly higher than that of the control group (75.87%, 305/402) [I2 = 0%, OR = 2.05, 95%CI: 1.39-3.03, P < 0.001]. The total remission rate of peptic ulcers across all allicin groups was 97.16%, which was significantly higher than that of controls [96.05% (389/405) vs 86.55% (360/402), I2 = 0, OR = 3.04, 95%CI: 1.51-6.12, P = 0.015]. No significant differences in side effects were observed. TSA suggested that the trials were of sufficient standard to draw reliable conclusions. The quality of outcomes including eradication rates and side effects was graded as “very low” due to downgrades for “risk of bias” and “indirectness”. Other outcomes such as ulcer healing rates and total ulcer remission rates were graded as "low" due to downgrades for “risk of bias”.CONCLUSIONAllicin as an add-on therapy improves H. pylori eradication, healing of ulcers, and remission of symptoms. These results are suggested to be treated with caution due to limited quality.

Allicin attenuates early brain injury after experimental subarachnoid hemorrhage in rats

Early Brain Injury, rather than Cerebral Vasospasm, has been demonstrated to be more important for patients with Subarachnoid hemorrhage. It is considered that allicin can make sense in a wide range of pharmacological areas and can be taken as a therapeutic method in many pathologic situations. We have explored the potential effect of allicin and possible mechanisms in Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats. With therapy (70 mg/kg Allicin, rather than 30 mg/kg) 30 min post SAH, groups showed better neurological scores in 24 h. Significant differences could be found in body weight ratio between the SAH + vehicle groups and SAH + Allicin groups. Treatment with 70 mg/kg, not 30 mg/kg, Allicin significantly reduced brain edema and EB extravasation in 24 h after SAH. Assessments in 24 h after SAH showed that treatment with 70 mg/kg Allicin in 30 min after SAH significantly restrained the expression of cleaved caspase-3, mitigated the severity of neuronal degeneration, decreased the proportion of apoptotic neurons and the elevated MDA levels, and increased the suppressed GSH and SOD levels. We demonstrated for the first time that Allicin extenuated brain edema and blood-brain barrier dysfunction, improved neurological outcomes by the suppression of apoptosis and oxidative stress damage after SAH in experimental models, which may shade new light on the treatments of SAH.

The effect of allicin on the ventricular myocytes of rabbit with heart failure

Objective To observe the effect of allicin on the action potential duration (APD) and L-type calcium current (ICa, L) in the ventricular myocytes of rabbits with heart failure in order to explore the mechanisms of therapeutic effect of allicin on cardiac arrhythmias complicated with heart failure. Methods Forty-five New Zealand White male rabbits were randomly (random number) assigned to 3 groups (n=15 in each group): sham operated group (sham group), heart failure group (HF group), and heart failure treated with allicin group (HF+All group). The rabbit heart failure model was established by abdominal aortic constriction coupled with aortic regurgitation, the ventricular myocytes were obtained by enzyme double digestion, and the whole cell clamp was used to record action potential and calcium current.The action potential duration (APD), ICa, L and gating mechanism were observed during heart failure and allicin administered. Data were processed with pCLAMP version 10.2. Statistical analysis was performed using SPSS 17.0. Comparisons among groups were carried out using ANOVA, and SNK-q was used for multiple comparison as post-hoc. Results (1) Prolonged APD was found during heart failure, APD50 was prolonged from (93.4±4.7) ms in sham group to (115.5±6.2) ms in HF group(P<0.01). After administration of allicin 30 μmol/L, APD50 was shortened to (105.2±5.5) ms (P<0.05). (2) The density of ICa,L increased during heart failure, peak current density increased increased from (-8.4±0.6) pA/pF in sham group to (-15.1±1.1) pA/pF while 0 mV attained at depolarizations (P<0.01). After administration of allicin 30 μmol/L, the current density reduced to (-10.1±0.8) pA/pF ( P<0.01). The effect of allicin presented in both voltage dependent and consentration dependent manner. (3) According to the gating mechanism study, the main mechanism of lowering the density of ICa, L by allicin after heart failure was the acceleration of the steady inactivation of the channel, and the de-escalation of the recovery kinetic after the inactivation of the channel. Conclusions Allcin can be used to reduce the calcium current of ventricular myocytes in animal heart failure model, it has the potential of clinical use in treating cardiac arrhythmias during heart failure. Key words: Allicin; Heart failure; Rabbit; Ventricular myocytes; Action potential; L- calcium current

Neuroprotective effects of allicin on ischemia-reperfusion brain injury.

BackgroundIschemia-reperfusion brain injury (IRBI) is an important cause for mortality and morbidity. Studies on humans and animals showed that oxidative stress (OS) plays a crucial role in ischemic stroke with or without reperfusion. Allicin is reported to be able to attenuate OS and has neuroprotective effects on rabbits’ ischemia–reperfusion spinal cord injury.AimTo explore whether Allicin pretreatment has neuroprotective effects on IRBI in mice.Methods and resultsTransient middle cerebral artery occlusion (MCAO) was conducted to induce IRBI in mice. The mice were pretreated with either Allicin (MCAOA) or normal saline in the same volume (MCAONS). Sham-operated groups [Allicin group (SOA) and normal saline group (SONS)] were also set. Blood pressure and cerebral blood flow measurements revealed comparable hemodynamics. Via brain MRI and neuronal nuclear antigen (NeuN) immune-histochemical staining, MCAOA mice had a significantly reduced stroke size than MCAONS mice (P < 0.05, n = 15). Allicin pretreatment could attenuate the OS, the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, inflammation, dysfunction of mitochondrial respiratory chain, and apoptosis (all P < 0.05, n = 15). Furthermore, Allicin also increased the activities of endogenous antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione S-transferase (GST), and promoted the angiogenesis in the peri-infarct zone (all P < 0.05, n = 15).ConclusionWe showed that Allicin could protect mice from IRBI through a series of mechanisms. Allicin represents a new therapeutic direction of IRBI.

Allicin improves carotid artery intima-media thickness in coronary artery disease patients with hyperhomocysteinemia.

Homocysteine (Hcy) is an important and independent risk factor for atherosclerotic diseases, such as coronary artery disease and ischemic cerebrovascular disease. Increased carotid artery intima-media thickness (IMT) is a non-invasive marker of systemic atherosclerosis. Allicin treatment may decrease serum Hcy levels and improve impaired endothelial function in rats with hyperhomocysteinemia (HHcy). The present study hypothesized that allicin has an anti-atherosclerotic effect in coronary heart disease and tested the effects of allicin treatment on carotid artery IMT and plasma Hcy levels in coronary heart disease patients with HHcy. Sixty-two coronary heart disease patients with HHcy were randomly divided into an allicin group and a control group. All patients underwent diagnostic assessment, plasma Hcy assay, blood lipid measurement and B-mode ultrasound of the carotid artery prior to and after treatment. Plasma Hcy levels were determined by high-performance liquid chromatography and fluorescence detection. Carotid artery IMT was calculated using an automated algorithm based on a validated edge-detection technique. After 12 weeks, significant decreases in carotid artery IMT, plasma Hcy levels, total cholesterol and triglycerides were observed in the allicin group (all P<0.05), and the decreases in the allicin group were significantly greater than those in the control group (all P<0.01). These findings suggested that reducing plasma Hcy levels may be useful for preventing the generation and development of atherosclerosis in patients with coronary heart disease. Allicin was able to decrease Hcy levels, total cholesterol and triglycerides as well as carotid artery IMT.

Allicin ameliorates intraintestinal bacterial translocation after trauma/hemorrhagic shock in rats: The role of mesenteric lymph node dendritic cell

Intestinal dendritic cells play important roles in regulating the function of the intestinal immune barrier and the intestinal bacterial translocation. In this study, we aim to investigate the effects of allicin on the function of mesenteric lymph node-dendritic cells after trauma/hemorrhagic shock. One hundred and eight-four Sprague-Dawley rats were randomly assigned into a sham group (n=46), sham+allicin group (n=46), trauma/hemorrhagic shock group (n=46), and trauma/hemorrhagic shock+allicin group (n=46). Studies were performed on an invivo model of spontaneously breathing rats with induced trauma/hemorrhagic shock. Allicin was diluted in resuscitation fluid and was administered through the right jugular vein. Flow cytometry was used to determine the expression of CD80, CD86, and major histocompatibility complex II (MHC II) on the surface of mesenteric lymph node-dendritic cells, as well as apoptosis. Intraintestinal bacterial translocation was monitored by using bioluminescent citrobacter. Intestinal permeability tests were conducted by using both FITC-Dextran and Ussing-Chember assay. CD80 and MHC-II expression levels were downregulated in the trauma/hemorrhagic shock group compared with the sham and sham+allicin groups; however, the expression was upregulated after allicin treatment. Also, allicin could ameliorate the trauma/hemorrhagic shock-induced increase in early apoptosis of mesenteric lymph node-dendritic cells. A significant increase was observed in the permeability of the intestinal barrier after severe traumatic shock, along with an obvious intraintestinal bacterial translocation to mesenteric lymph node. No difference was noticed in the bacterial translocation in mesenteric lymph node in the trauma/hemorrhagic shock group compared with trauma/hemorrhagic shock+allicin group (P=.589), which indicated allicin could not block bacterial translocation into mesenteric lymph node after trauma/hemorrhagic shock. However, it may increase the capacity of mesenteric lymph node to block intraintestinal bacterial translocation to extraintestinal organs as a statistical difference was noticed in the bacterial translocation in liver, blood, and spleen between trauma/hemorrhagic shock and trauma/hemorrhagic shock+allicin groups (P<.05). Trauma/hemorrhagic shock resulted in a decrease of mature mesenteric lymph node-dendritic cells. Allicin treatment could block intraintestinal bacterial translocation through increasing the immunologic barrier function of mesenteric lymph node by modulating dendritic cells maturation.

Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction.

To study the effects of allicin on cardiac function and underlying mechanism in rat model of myocardial infarction (MI). Ninety-four Wistar rats were randomly assigned to 6 groups (n=14-16 per group): sham control group [underwent thoracotomy without left anterior descending (LAD) occlusion and only received an injection of the same amount of citrate buffer], MI control group (subjected to LAD occlusion and only received an injection of same amount of citrate buffer), positive control group (subjected to LAD occlusion and received an injection of diltiazem hydrochloride at the dose of 1.5 mg/kg), and MI + allicin groups (subjected to LAD occlusion and received an injection of allicin at the doses of 1.2, 1.8, and 3.6 mg/kg). All of the drugs were administered intraperitoneally daily for 21 days. The infarct area was measured by myocardial staining. Hematoxylin-eosin staining was used to observe the pathological changes. Cardiac function parameters were assessed by echocardiography. The myocardial apoptotic index was estimated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining. The expression of Bax and Bcl-2 were detected by quantificational real-time polymerase chain reaction and Western blot. Treatment with allicin could attenuate the myocardial infarct area (P<0.05) and relieve the changes of the myocardium. The left ventricular anterior wall diastolic and systolic thicknesses were increased in the allicin-treated groups (P<0.05), while there was no signifificant difference in the left ventricular posterior wall diastolic and systolic thickness (P>0.05). The left ventricular internal diameter in systole, ejection fraction, fractional shortening, and stroke volume were dramatically elevated in allicin-treated rats (P<0.05). Allicin dose-dependently reduced creatine kinase and lactate dehydrogenase levels (P<0.05). The myocardial apoptotic index was also markedly lowered, and Bax expression was signifificantly decreased, whereas Bcl-2 expression exhibited an opposite trend in allicin-treated rats (P<0.05). Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis, further improving cardiac function.

Inhibition of allicin in Eca109 and EC9706 cells via G2/M phase arrest and mitochondrial apoptosis pathway

The effects and underlying molecular mechanisms of allicin on oesophageal squamous cell carcinoma (ESCC) are unclear. Herein, we investigated the effect and action mechanism of allicin in the ESCC cells of Eca-109 and EC9706. The cell viability and invasion ability of the two ESCC cells in allicin group were significantly decreased after allicin treatment. Allicin reduced the percentage of G0/G1 and S phase and increased the population of G2/M phase in a dose-dependent manner. The expression levels were significantly increased for p53, p21, CHK1, and decreased for cyclinB after allicin treatment. The apoptotic rate was significantly increased and accompanied by Cyt c release from the mitochondria to the cytosol, as well as Bax, caspase-3 and cleaved caspase-9 which were significantly increased. Furthermore, suppression of tumour growth was evident in vivo. These results suggest that allicin can serve as a novel and effective anti-oesophageal cancer agent for the treatment of ESCC.

Effect of allicin on myocardial fibrosis after myocardial infarction in rats and its relationship with TGFβ/Smads signal transduction

Allicin is the internationally accepted active substance of garlic, and has cardiovascular protective effect. This research was designed to investigate the effect of allicin on myocardial fibrosis after myocardial infarction and explore the relationship between the effect and TGFβ1/Smads signaling pathway. The rat myocardial infarction model were made by ligating the left anterior desending coronary artery. The drugs were administered intraperitoneally 24 h after the operation. After 21 days, the rats were sacrificed and myocardial collagen fibres were observed by Masson staining. The protein expression of Ⅰ, Ⅲ collagen and TGFβ1, Smad3, Smad7 in the myocardium was measured by the immunohistochemistry. The results showed that myocardial fibrosis was serious and the expression of Ⅰ, Ⅲ collagen was increased in model group. After treatment with allicin, the myocardial fibrosis could be relieved markedly, and the expression of collagen was down-regulated. Meanwhile, TGFβ1 and Smad3 in heart tissue could be down-regulated and Smad7 could be up-regulated in allicin groups. So allicin may exhibit anti-myocardial fibrosis effect on rats, and the mechanism of this is related to TGFβ/Smads signal transduction.

Protective effect of allicin on high glucose/hypoxia-induced aortic endothelial cells via reduction of oxidative stress

This study was designed to explore the protective effect of allicin on aortic endothelial cell injury induced by high glucose/hypoxia and to investigate the corresponding mechanisms. The primary-cultured murine aortic endothelial cells were subcultured. The third passage of cells was adopted and randomly divided into five groups: The normal group (NG), the mannitol group (MG), the high-glucose/hypoxia group (HG), the allicin group (AG) and the protein kinase C (PKC) inhibitor group (GG). The general morphology was observed under an inverted phase-contrast microscope and cell viability was assessed using the MTT assay. Intracellular reactive oxygen species (ROS) levels in the endothelial cells were quantified using dihydroethidium staining. The levels of 8-hydroxydeoxyguanosine (8-OHdG), nuclear factor-κB (NF-κB), NADPH oxidase 4 (Nox4) and hypoxia-inducible factor-1α (HIF-1α) and the activity of PKC were measured using ELISA. A quantitative polymerase chain reaction (qPCR) was adopted to evaluate the mRNA expression of Nox4, HIF-1α and NF-κB. The altered cell morphology observed in HG was notably ameliorated in the AG and GG. The protein levels of 8-OHdG, NF-κB, Nox4, HIF-1α and PKC in the HG were higher than those in the other groups. Furthermore, the cell viability in the AG was significantly increased and the protein levels of 8-OHdG, NF-κB, Nox4, HIF-1α and PKC were significantly decreased compared with those in the HG. The ROS production was found to be increased in the HG cells, while there was a significant decrease in the AG cells. These data indicate that allicin exerts a protective effect against high glucose/hypoxia-induced injury in aortic endothelial cells through its antioxidative action, which may involve the inhibition of the PKC pathway and regulation of HIF-1α.

Allicin as a possible adjunctive therapeutic drug for stage II oral submucous fibrosis: a preliminary clinical trial in a Chinese cohort

The objective of this study was to investigate the efficacy and safety of allicin in the treatment of stage II oral submucous fibrosis (OSF) in a Chinese patient cohort. A randomized clinical trial was performed. Triamcinolone acetonide (TA) or allicin was injected intralesionally weekly for 16 weeks. Improvements in mouth opening, burning sensation, and oral health-related quality of life were evaluated. Forty-eight subjects completed the study without obvious adverse reactions. At 40 weeks, the net gain in mouth opening was 2.27±0.84mm in the TA group and 5.16±1.04mm in the allicin group. Burning sensation improved by 2.79±0.87 in the TA group and by 4.33±1.04 in the allicin group. The OHIP-14 score improved by 4.67±2.94 in the TA group and by 12.58±9.82 in the allicin group. Allicin intralesional injections improved mouth opening, burning sensation, and oral health-related quality of life in these stage II OSF patients. Allicin appears to be a potential adjunctive therapeutic drug.

Protective effects of allicin against ischemic stroke in a rat model of middle cerebral artery occlusion.

Allicin, a molecule predominantly responsible for the pungent odor and the antibiotic function of garlic, exhibits various pharmacological activities and has been suggested to be beneficial in the treatment of various disorders. The present study aimed to elucidate the effect of allicin in cerebral ischemia/reperfusion (I/R) injury in rats. Rats were subjected to 1.5 h of transient middle cerebral artery occlusion (MCAO), followed by 24 h of reperfusion. Rats were randomly assigned to the sham surgery group, the MCAO group and the MCAO + allicin group. Neurological score, cerebral infarct size, brain water content, neuronal apoptosis, serum tumor necrosis factor (TNF)‑α and myeloperoxidase (MPO) activity were measured. The results suggested that allicin reduced cerebral infarction area, brain water content, neuronal apoptosis, TNF‑α levels and MPO activity in the serum. The results of the present study indicated that allicin protects the brain from cerebral I/R injury, which may be ascribed to its anti‑apoptotic and anti‑inflammatory effects.

Experimental study on effect of allicin in inhibiting insulin-induced vascular smooth muscle cell proliferation and migration

To investigate the effect of allicin in inhibiting insulin-induced vascular smooth muscle cell (VSMC) proliferation and migration. The tissue explant method was adopted to culture rat's aVSMCs, and the immunofluorescence method was used to identify α-SMA. Cells from the third to fifth generations were selected in the experiment The insulin-induced VSMC model was established. The experiment was carried out in five groups: the control group, the insulin group, the allicin group, the ERK inhibitors PD98059 group (20 μmol · L(-1)) and the PD98059 + allicin group. VSMCs' proliferation was determined by CCK8 colorimetric method, while its migration was detected by cell counting; The western blotting was used to detect total ERK, Phospho-ERK, PCNA protein's expression. Primary cultured VSMCs grew well in the spindle shape under the lightmicroscope, with peak and valley. α-SMA immunofluorescence results showed that the cultured cells had typical VSMCs' features. Insulin could stimulate VSMCs' proliferation and migration, with the best effect at the concentration of 100 nmol · L(-1). The pretreatment with allicin could significantly inhibit VSMCs' proliferation and migration induced by insulin in a dose-dependent manner. The pretreatment with PD98059 and allicin + PD98059 could inhibit VSMCs' proliferation and migration induced by insulin remarkably as well. Insulin could significantly accelerate VSMCs' expression of such proteins as p-ERK, PCNA. Contrarily, allicin could notably inhibit VSMCs' expression of such proteins as p-ERK, PCNA in a dose-dependent manner. Allicin could significantly inhibit VSMCs' proliferation and migration induced by insulin, which may be related to the inhibition of the activation of ERK signal path.

Effect of combined treatment with recombinant interleukin-2 and allicin on pancreatic cancer

This study aimed to evaluate the efficacy of combined treatment with recombinant interleukin-2 (rIL-2) and allicin on pancreatic cancer and explore the potential immunological mechanism. A total of 60 C57/BL6 nude mice pancreatic cancer xenograft models were randomized into four groups of 15 mice per group: control group, allicin treatment group, rIL-2 treatment group, combined treatment with allicin and rIL-2 group. Mice in each group were treated with saline, rIL-2, allicin, or combination of rIL-2 and allicin by weekly i.v injection for four weeks. After four weeks of treatment, eyeballs of the mice were extracted and blood was drawn, percentages of CD4+T, CD8+T and NK cell were analyzed by FACS, IFN-γ level was detected by ELISA. One mouse in each group was sacrificed to measure the weight and volume of the tumor and prepared to the paraffin section of tumor tissue. Apoptosis of the tumor cells was analyzed by TUNEL and FACS. Other mice continued to receive treatment, survival period were compared between each group. We observed a significant suppression of xenograft growth and a significant prolonged survival time in the combined treatment with allicin and rIL-2 group (P<0.05). The most amount of apoptotic cells were observed in the combined therapy group (P<0.05). The percentages of CD4+T, CD8+T and NK cell and serum IFN-γ level increased significantly in the combined treatment group compared with other groups (P<0.05). Combined treatment with allicin and rIL-2 resulted in suppression of tumor growth and prolonged survival time possibly through activation of CD4+T, CD8+T and NK cell.

Allicin Ameliorates Cardiac Hypertrophy and Fibrosis through Enhancing of Nrf2 Antioxidant Signaling Pathways

To evaluate the protective effects of allicin on Ang II-induced cardiac hypertrophy. Sprague-Dawley male rats were randomized into 3 groups:1)sham group (saline)(n = 12), 2) Ang II group(n = 9), 3) allicin group (Ang II + allicin)(n = 9). They received infusions of either saline or Ang II (250 ng/kg body weight per min) through mini-osmotic pumps implanted subcutaneously for 2 weeks and given a diet containing 180 mg/kg/day of allicin for 8 consecutive weeks. Hemodynamic, morphological, histological, and biochemical changes were evaluated at corresponding time points. Ang II infusion increased blood pressure, heart rate and heart weight to body weight ratio, and resulted in anatomical and functional changes, such as increased LV mass, posterior wall thickness and LV end-diastolic diameter, and decreased fractional shortening and EF compared with sham rats. Nrf2 and HO-1 in the hearts of rats in the Ang II group were moderately elevated at both mRNA and protein levels compared to sham group mice, but NQO1 andγ-GCS were significantly lower. GPx activities, levels of GSH and T-AOC in the hearts of the rats in the Ang II group were also significantly lower, and the levels of TBARS, reactive oxygen species and protein carbonyl were significant increased. Allicin attenuated LV mass, posterior wall thickness and LV end-diastolic diameter (1.10 ± 0.04 vs. 1.37 ± 0.05, 2.26 ± 0.08 vs. 2.96 ± 0.12, 7.27 ± 0.36 vs. 8.56 ± 0.41, respectively; all P < 0.05), and increased fractional shortening and EF (28.30 ± 3.21 vs. 25.40 ± 2.57, 60.27 ± 5.63 vs. 51.30 ± 4.78, respectively; both P < 0.05) in the Ang II-induced hypertrophic rats compared to the untreated Ang II rats. Furthermore, allicin treatment attenuated the accumulation of interstitial collagen and collagen I/III (P < 0.01 vs. the untreated Ang II group), decreased the levels of reactive oxygen species, protein carbonyl and TBARS and increased GPx activities. Moreover, allicin significantly increased mRNA expression and protein levels of Nrf2, NQO1, and γ-GCS ( P < 0.01, P < 0.05 vs. the untreated Ang II group). Allicin could prevent the development of cardiac remodeling and the progression of cardiac hypertrophy to cardiac dysfunction caused by enhancing the Nrf2 antioxidant signaling pathways.

The studies of allicin combined with meropenem against carbapenem-resistant Acinetobacter baumannii in vitro

Objective To investigate in vitro meropenem combined with allicin for carbapenem-resistant Acinetobacter baumannii in the sterilization.Methods (1)Using EDTA-Na2 paper composite method and improved three-dimensional experiments on more than six-resistant Acinetobacter baumannii to identify produce metal β-lactamase enzymes.(2)M-H broth method was used to determine the allicin,meropenem,allicin + meropenem MIC values,calculated the FIC index of two drugs combined with.K-B disk diffusion method identification of allicin on meropenem antibacterial effects,the allicin,meropenem and the two drugs combined with inhibitory rate were used the bio-detection microplate assay.(3)The glutathione on the impact of antimicrobial effect of allicin were madedetection by M-H broth，and the change of glutathione,anti-superoxide anion radical and total thiol were measured after different concentrations of allicin incubation.(4)Improved three-dimensional experiments and MH broth assayed the role of allicin on the metal β-lactamase enzymes decomposing carbapenem antibiotic.Results (1)All six-resistant Acinetobacter baumannii produced metal β-lactamase enzymes were identified by EDTA-Na2 paper composite method and improved three-dimensional experiments.(2)Allicin and meropenem on six carbapenem-resistant Acinetobacter baumannii antibiotic MIC values were 512 μg/ml and 128 μg/ml.FIC of the two drugs together with was 025,the sterilization role of allicin+meropenem were more than either drug alone.(3)The inhibition on bacterials were significantly decreased in 03 mg/ml GSH + different concentrations of allicin groups compared with allicin groups.The glutathione,anti-superoxide anion radical,and total thiol were decreased significantly after different concentrations of allicin application,and high allicin concentrations groups were lower than concentrations of allicin.(4)The effects of meropenem antibacterial was significantly increased in allicin +the enzyme extract group compared with enzyme extract groups.Conclusions The role of allicin inhibiting carbapenem-resistant Acinetobacter baumannii caused the bacterial oxidative imbalance.The combined use of allicin and meropenem has a synergistic effect on the bacteria,the mechanism may be related to allicin inhibited metal β-lactamase enzyme.