S-allylcysteine Research Articles

An evaluation of garlic products available in Australian pharmacies–From the label to the laboratory

Garlic is one of the most commonly used herbal medicines worldwide. There is medium quality evidence to support that specific garlic formulations at specific doses have an antihypertensive effect in a cohort of individuals with hypertension. There is lower quality evidence for garlic’s hypolipidaemic effects. While there are many garlic products available in Australian pharmacies, it is unclear if these products are formulated based on the current evidence for use in such populations. The aim of this study was to evaluate garlic product formulations available in Australian pharmacies for quality indicators including: supporting evidence, labelling, product, safety and manufacturing information and the presence of key constituents previously identified as having hypotensive or hypolipidaemic properties. A qualitative evaluation of commercially available garlic products was conducted in accordance with the study aims. Thin-layer chromatography (TLC) was included in the evaluation to investigate the presence of alliin and s-allyl cysteine in both garlic products and raw garlic. The quality indicators evaluated in this study including evidence for the formulation used, labelling, product, safety and manufacturing information and key constituents varied significantly between the garlic products available in Australian pharmacies. These findings have a number of implications that relate to the formulations and doses chosen by herbalists, pharmacists and consumers who may consider using garlic products in the management of hypertension and/or dyslipidaemia.

Organosulfur compounds induce cytoprotective autophagy against apoptosis by inhibiting mTOR phosphorylation activity in macrophages.

Organosulfur compounds (OSCs) are the bioactive components of garlic. Some OSCs have apoptotic or autophagy-inducing effects. Autophagy plays roles in both cytoprotection and apoptosis-related cell death, and the interaction between autophagy and apoptosis is important in the modulation of immune responses. The mechanism of an OSC-mediated effect via the interaction of autophagy and apoptosis is unknown. In this study, the effects of five OSC compounds on autophagy in the macrophage cell line RAW264.7 and primary macrophages were investigated. We found that S-allylcysteine (SAC), diallyl disulde (DADS) and diallyl tetrasulfide (DTS) treatment increased the number of autophagosomes of RAW264.7 cells, inhibited the phosphorylation of ribosomal protein S6 kinase beta-1 (p70S6K/S6K1) which is a substrate of mammalian target of rapamycin (mTOR), and significantly enhanced autophagy flux. The induction of autophagy by SAC, DADS and DTS was inhibited by stably knocking down the expression of autophagy-related gene 5 (ATG5) with short hairpin RNA (shRNA). Further experiments confirmed that SAC, DADS and DTS also induced apoptosis in RAW264.7 cells. The induction of apoptosis and Caspase 3 activity by SAC, DADS and DTS were increased by stably knocking down of ATG5 expression with shRNA in RAW264.7 cells or treating with 5 mM 3-MA in primary macrophages. Our results suggest that SAC, DADS and DTS induce both autophagy and apoptosis. The autophagy induction protects macrophages from apoptosis by inhibiting mTOR phosphorylation activity to maintain the mass of immune cells.

Restorative potentiality of S-allylcysteine against diabetic nephropathy through attenuation of oxidative stress and inflammation in streptozotocin-nicotinamide-induced diabetic rats.

In the present study, we evaluated the therapeutic potentiality of S-allylcysteine (SAC) in streptozotocin (STZ)-nicotinamide (NAD)-induced diabetic nephropathy (DN) in experimental rats. SAC was orally administered for 45days to rats with STZ-NAD-induced DN; a metformin-treated group was included for comparison. Effect of SAC on body weight, organ weight, blood glucose, levels of insulin, glycated haemoglobin, and renal biochemical markers was determined. Body composition by total body electrical conductivity (TOBEC) and dual-X ray absorptiometry (DXA), kidney antioxidant analysis, real-time polymerase chain reaction, and western blot analysis of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), nuclear factor kappa B (NF-κB), interleukin (IL)-6, and tumor necrosis factor (TNF)-α; histopathological and scanning electron microscope (SEM) analysis of the kidneys were performed in both control and experimental rats. SAC treatment showed significantly decreased levels of blood glucose, glycated haemoglobin, creatinine, albumin, AST, ALT, creatinine kinase, lactate dehydrogenase, and expressions of NF-κB, IL-6, and TNF-α compared with DN control rats. Furthermore, SAC administration to DN rats significantly improved body composition and antioxidant defense mechanism which was confirmed by the upregulation of mRNA and protein expressions of antioxidant genes. Thus, SAC showed adequate therapeutic effect against DN by downregulation of inflammatory factors and attenuation of oxidative stress. Histological and SEM observations also indicated that SAC treatment notably reverses renal damage and protects the kidneys from hyperglycemia-mediated oxidative damage.

S-allyl cysteine as potent anti-gout drug: Insight into the xanthine oxidase inhibition and anti-inflammatory activity

S-allyl cysteine (SAC) is known for its various beneficial effects such as neuroprotection and immunomodulation. The beneficial effect of SAC against gout has not been explored. The present study aims to describe the two roles of SAC: (1) inhibitory effect against xanthine oxidase (XO) enzyme activity; and (2) anti-inflammatory property against MSU crystal-induced gouty inflammation in rat. The inhibitory effect of SAC against bovine XO enzyme activity was determined in vitro. In silico analysis was carried out to determine the intermolecular interaction between SAC and bovine XO. MSU crystal was injected in the right paw of the rat to induce gouty inflammation. SAC (40 mg/kg body weight) and colchicine (positive control; 1 mg/kg body weight) was given for 3 days. At the end of the treatment, the oxidative stress, antioxidant parameters and mitochondrial function were determined in the ankle joint tissue. The concentration of inflammatory cytokines such as TNF-α and IL-1β was measured in the serum using ELISA. SAC inhibited (IC50 value, 33 μg/ml) XO enzyme activity in a competitive mode with corresponding Ki value of 4 μg/ml. In silico analysis predicted the interaction of SAC with the amino acids such as Arg880, Phe798, Phe914 and Phe1009 of XO enzyme. The root mean square deviation, root mean square fluctuation and free energy calculation values confirmed the stable SAC-XO interaction. The inhibition of SAC on XO enzyme activity in in vivo was further confirmed by silkworm model. SAC through reducing oxidative stress, enhancing antioxidants, protecting mitochondrial function has shown anti-inflammatory effect against MSU crystal-induced gout which was observed as reduced level of inflammatory markers in the serum. The medicinal potential of SAC as a preventive agent through its XO inhibitory property as well as curative agent through its anti-inflammatory property against gout has been understood from the present study.

Effects of S-Allyl Cysteine on Insulin Secretion: A Proposed Mechanism for its Anti-Hyperglycemic Effects

Effects of S-Allyl Cysteine on Insulin Secretion: A Proposed Mechanism for its Anti-Hyperglycemic Effects

S-allyl cysteine ameliorates cyclophosphamide-induced downregulation of urothelial uroplakin IIIa with a concomitant effect on expression and release of CCL11and TNF-α in mice.

The aim of this study was to evaluate the modulatory effect of S-allyl cysteine against cyclophosphamide-induced changes in uroplakin IIIa, CCL11 and TNF-α. Mice were treated with cyclophosphamide (200mg/kg×7 d, ip). S-allyl cysteine (150mg/kg×7d, ip), and comparator compound mesna (40mg/kg×7d, ip) were administered 1h before and 4h after each cyclophosphamide dose. The urinary bladder was analysed for mRNA and protein changes in uroplakin IIIa (UPIIIa), CCL11 and TNF-α and histopathological findings. Cyclophosphamide caused hemorrhagic cystitis formation and downregulation of UPIIIa. These changes were accompanied by upregulation of CCL11 and TNF-α. S-allyl cysteine attenuated these changes including protection at histological level. Mesna which was used as a comparator drug also showed protection. However, relatively S-allyl cysteine showed a stronger protective effect than mesna. These findings highlight a correlation between downregulaion of UPIIIa and enhanced production of inflammatory biomarkers and protective effects of S-allyl cysteine which has been reported to be a potent uroprotective agent. The present study strengthens its role which could be clinically exploited in chemotherapy regimen.

Biological interaction of newly synthesized astaxanthin-s-allyl cysteine biconjugate with Saccharomyces cerevisiae and mammalian α-glucosidase: In vitro kinetics and in silico docking analysis

In humans, alpha-glucosidase activity is present in sucrase-isomaltase (SI) and maltase-glucoamylase (MGAM). α-glucosidase is involved in the hydrolyses of disaccharide into monosaccharides and results in hyperglycemia. Subsequently chronic hyperglycemia induces oxidative stress and ultimately leads to the secondary complications of diabetes. Hence, identifying compounds with dual beneficial activity such as efficient antioxidant and α-glucosidase inhibition property has attracted the attention in recent years. Keeping these views, in the present study astaxanthin (AST; a natural antioxidant present in marine microalgae) was biconjugated with allyl sulfur amino acid such as s-allyl cysteine (SAC). The synthesized AST-SAC (with molecular weight of 883.28) was characterized using UV–visible spectrophotometer, ESI-MS, and NMR analysis. AST-SAC showed potent antioxidant property in vitro. AST-SAC inhibited Saccharomyces cerevisiae α-glucosidase (IC50 = 3.98 μM; Ki = 1 μM) and mammalian α-glucosidase [rat intestinal maltase (IC50 = 6.4 μM; Ki = 1.3 μM) and sucrase (IC50 = 1.6 μM; Ki = 0.18 μM)] enzyme activity in a dose-dependent manner. Kinetic analysis revealed that AST-SAC inhibited all the α-glucosidases in a competitive mode. In silico analysis determined the interaction of AST-SAC with the amino acids present in the active site of S. cerevisiae and human (MGAM and SI) α-glucosidases.

S-allylcysteine suppresses ovarian cancer cell proliferation by DNA methylation through DNMT1

BackgroundThe anti-tumor effects of S-allylcysteine (SAC), a water-soluble garlic derivative, on human ovarian cancer cells have been previous studied in vitro and in vivo models but the precise epigenetic molecular mechanisms are still unclear. This study aimed to investigate the epigenetic mechanism of SAC.MethodsHuman epithelial ovarian cancer cell line A2780 was selected. Cell proliferation and cell cycle was analyzed. DNA methylation, DNA methyltransferase (DNMT) activity, tumor suppressor gene expressions, as well as protein expression were analyzed.ResultsSAC could inhibit the proliferation of A2780 cells in dose- and time-dependent manners (the IC50 was 16.25 mmol/L and 5.25 mmol/L at 48 h and 72 h). Treatment of A2780 cells with SAC resulted in G1/S phase arrest. SAC treatment decreased global DNA methylation levels in A2780 cells in a dose-dependent manner. SAC decreased the levels of 5-methylcytosine, DNMT activity, messenger RNA (mRNA) and protein levels of DNMT1. Additionally, SAC treatment resulted in re-expression of the mRNA and proteins of silenced tumor suppressor gene CDKN1A accompany with reduced cell division control 2 expression.ConclusionOur data indicated the potential therapeutic effects of SAC on the human ovarian carcinoma cell line A2780 in vitro. The epigenetic mechanism of action of SAC may have important implications for epigenetic therapy.

Insulinotropic Effect of S-Allyl Cysteine in Rat Pups.

S-Allyl cysteine (SAC) is found in garlic and has been reported to exert antidiabetic and antiobesity properties in drug-induced adult experimental models of metabolic dysfunction, but its potential beneficial effects in high-fructose diet neonatal rat models have not been determined. This study investigated the potential prophylactic effects of SAC in high-fructose diet fed suckling rat pups modelling human neonates fed a high-fructose diet. Four-day-old male (n=32) and female (n=32) Wistar rat pups, were randomly assigned to and administered the following treatment regimens daily for 15 days: group I, distilled water; group II, 20% fructose solution (FS); group III, SAC; group IV, SAC+FS. The pups’ blood glucose, triglyceride, cholesterol, plasma leptin and insulin concentration, liver lipid content, and liver histology were determined at termination. In female rat pups, orally administered SAC prevented FS-induced hypoinsulinemia but significantly increased (P≤0.05) liver lipid content. Oral administration of SAC significantly increased (P≤0.05) plasma insulin concentration and homeostasis model assessment for insulin resistance in the male pups. The potential sexually dimorphic effects of SAC (insulinotropic effects in male pups and protection of female pups against fructose-induced hypoinsulinemia) suggest that SAC could be potentially exploited as an antidiabetic and insulinotropic agent. Caution should, however, be exercised in the use of SAC during suckling as it could result in excessive liver lipid accumulation and insulin resistance.

EFFECT OF EXTRACTION CONDITIONS ON POLYPHENOLS, FLAVONOIDS, S-ALLYL CYSTEINE CONTENT AND ANTIOXIDANT ACTIVITY OF BLACK GARLIC EXTRACTS

Black garlic is obtained from fresh garlic (Allium sativum L.) that has been aged for a long time at a high temperature under high humidity. Black garlic exerts metabolic and cardiovascular beneficial effects. In this study, (i) water and various concentrations of ethanol (50 % and 100 %) in water were used as solvent in the extraction of black garlic with different black garlic:solvent ratios (1:5, 1:10 and 1:15 w/v); (ii) the process was investigated in the temperatures ranging of 40 to 80 oC during 30 to 120 minutes, as well as determination of bioactive compounds content (total polyphenols, total flavonoids and S-allyl cysteine content) of all obtained extracts. The antioxidant activity was evaluated by DPPH (2,2-diphenyl-1-picrylhydrazyl) radical scavenging activity. The obtained results indicated that the aqueous ethanol (50 %) extracts presented the highest contents of polyphenols and flavonoids (7.94 mg GAE/g and 3.37 mg QE/g, respectively) and DPPH radical scavenging activity at black garlic: solvent ratio of 1:10 (w/v); while the water extract showed the highest S-allyl cysteine content (76.0 mg/kg) at the 1:10 ratio. The suitable condition for extracting of total polyphenols and flavonoids from black garlic was 60 oC for 90 minutes. With respect to SAC extraction, the suitable temperature and time of 80 oC and 90-120 minutes, respectively were found.

Hypoglycemic and hypolipidemic effect of S-allyl-cysteine sulfoxide (alliin) in DIO mice

Alliin (S-allyl cysteine sulfoxide) is a bioactive sulfoxide compound derived from garlic. To evaluate the preventive effect of alliin against metabolic risk factors in diet induced obese (DIO) mice, we treated the C57BL/6J DIO mice with drinking water with or without alliin (0.1 mg/ml) for 8 weeks. Results showed that alliin had no significant effect on the body weight, adiposity or energy balance. However, alliin treatment enhanced glucose homeostasis, increased insulin sensitivity and improved the lipid profile in the DIO mice. This was, at least partly, attributable to alliin induced modulation of the intestinal microbiota composition, typically decreased Lachnospiraceae and increased Ruminococcaceae. From above, we conclude that alliin has nutraceutical or even medicinal potential in prevention of diabetes and lipid metabolic disorders.

Organo-Sulphur Garlic Compounds Influence Viability of Mammalian Cells: A Review

Abstract Garlic is still in the centre of interest for its therapeutic effects. Currently, attention is focused on physiological effects of organo-sulphur garlic compounds, as alliin, allicin, diallyl sulfide (DAS), diallyl disulfide (DADS), diallyl trisulfide (DATS), and S-allyl cysteine (SAC), particularly on their antioxidant and anticancerogenic effects. SAC has been studied for its ability to decrease the production of reactive oxygen species by modulation of the cell glutathione level together with antioxidative enzyme activity, and by improvement of mitochondrial functions. The main mechanism of DAS, DADS, and DATS is the induction of the internal apoptotic pathway. Garlic compounds have the ability to interfere with the signalling pathways of small gaseous signalling molecules known as gasotransmitters – nitric oxide, hydrogen sulfide, and carbon monoxide. The review presents the effect of garlic compounds on cellular oxidative stress, intrinsic apoptotic and gasotransmitter pathways and compares their effects on tumour and normal mammalian cells.

Neuroprotective effect of S-allyl cysteine on an experimental model of multiple sclerosis: Antioxidant effects

S-allyl cysteine (SAC), has shown itself to performance important activity as a neuroprotective agent. This action is prompted by antioxidative activity. The aim of this study was to evaluate the neuroprotective effect of SAC, the principal organosulfur compound of garlic, on experimental autoimmune encephalomyelitis (EAE) as a model of multiple sclerosis (MS). Young-adult Dark Agouti rats were used. The experimental model of EAE was carried out by means of mielyn oligodendrocyte glycoprotein (MOG). The effects of MOG were evaluated by changes in: clinical score, biomarkers of oxidative/nitrosative stress, antioxidants, mitochondrial viability and neurohistologic viability. Our results reveal that MOG causes oxidative/nitrosative damage in brain and spinal cord, a decrease in the glutathione redox system and cell loss, whereas SAC administration attenuates the effects of MOG. In addition, SAC was the most effective treatment used in this study. The data show the ability of SAC to modify the development of EAE.

S-allyl cysteine inhibits TNFα-induced skeletal muscle wasting through suppressing proteolysis and expression of inflammatory molecules

BackgroundElevated levels of inflammatory molecules are key players in muscle wasting/atrophy leading to human morbidity. TNFα is a well-known pro-inflammatory cytokine implicated in the pathogenesis of muscle wasting under diverse clinical settings. S-allyl cysteine (SAC), an active component of garlic (Allium sativum), has established anti-oxidant and anti-inflammatory effects in various cell types. However, the impact of SAC on skeletal muscle pathology remains unexplored. Owing to the known anti-inflammatory properties of SAC, we investigated whether pre-treatment with SAC has a protective role in TNFα-induced atrophy in cultured myotubes. Methods and resultsC2C12 myotubes were treated with TNFα (100ng/ml) in the presence or absence of SAC (0.01mM). TNFα treatment induced atrophy in myotubes by up-regulating various proteolytic systems i.e. cathepsin L, calpain, ubiquitin-proteasome E3-ligases (MuRF1/atrogin1), caspase 3 and autophagy (Beclin1/LC3B). TNFα also induced the activation of NFκB by stimulating the degradation of IκBα (inhibitor of NFκB), in myotubes. The alterations in proteolytic systems likely contribute to the degradation of muscle-specific proteins and reduce the myotube length, diameter and fusion index. The SAC supplementation significantly impedes TNFα-induced protein loss and protects myotube morphology by suppressing protein catabolic systems and endogenous level of inflammatory molecules namely TNFα, IL-6, IL-1β, TNF-like weak inducer of apoptosis (TWEAK), fibroblast growth factor-inducible 14 (Fn14) and Nox. Conclusion and general significanceOur findings reveal anti-atrophic role for SAC, as it prevents alterations in protein metabolism and protects myotubes by regulating the level of inflammatory molecules and multiple proteolytic systems responsible for muscle atrophy.

Effect of neonatal orally administered S-allyl cysteine in high-fructose diet fed Wistar rats.

S-allyl cysteine (SAC) has antioxidant, antidiabetic and antiobesity properties. We hypothesized that neonatal oral administration of SAC would protect rats against neonatal and adulthood high-fructose diet-induced adverse metabolic outcomes in adulthood. In total, 112 (males=56; females=56), 4-day-old Wistar rat pups were randomly allocated to groups and administered the following treatment regimens daily for 15 days from postnatal day (PND) 6-20: group I - 10 ml/kg distilled water, group II - 10 ml/kg 20% fructose solution (FS), group III - 150 mg/kg SAC and group IV - SAC+FS. On PND 21, the pups were weaned and allowed to grow on a standard rat chow (SRC) until PND 56. The rats from each treatment regimen were then randomly split into two subgroups: one on a SRC and plain drinking water and another on SRC and 20% FS as drinking fluid and then subjected to these treatment regimens for 8 weeks after which they were euthanized and tissues collected for analyzes. Neonatal oral administration of SAC attenuated the neonatal high-fructose diet-induced programming for hepatic lipid accretion in adulthood but not against adulthood high-fructose diet-induced visceral obesity. Neonatal oral administration of SAC programmes for protection against neonatal fructose-induced programming for hepatic lipid accumulation thus could potentially protect against fat-mediated liver derangements in adult life.

S-allyl cysteine improves clinical and neuropathological features of experimental autoimmune encephalomyelitis in C57BL/6 mice

Multiple sclerosis (MS) is a deleterious autoimmune and demyelinating disorder of the central nervous system with debilitating sensory and motor complications. There is still no definite cure for it and the main focus for its treatment mostly pivots around subsiding its severity and recurrence. Experimental autoimmune encephalomyelitis (EAE) is an established animal model of MS. S-allyl cysteine (SAC) is the active and main constituent of aged garlic extract with anti-inflammatory and neuroprotective property. This study was conducted to evaluate its possible protective effect in EAE model of MS. SAC was administered p.o. at a dose of 50 mg/kg/day to female C57BL/6 mice immunized with myelin oligodendrocytic glycoprotein (MOG35-55). Results showed that SAC is capable to alleviate clinical signs and severity of the disease and improved lumbar spinal cord tissue level of tumor necrosis factor α (TNFa), interleukin 17 (IL-17), activity-dependent neuroprotector homeobox (ADNP), microtubule-associated proteins 1A/1 B light chain 3A (MAP1LC3A), and matrix metalloproteinase 9 (MMP-9). In addition, SAC attenuated inflammatory cell infiltration, axonal demyelination, and axonal loss in lumbar spinal cord in EAE group, as demonstrated by H & E, Luxol fast blue (LFB), and Bielschowsky silver staining, respectively. Taken together, SAC could mitigate severity of MOG35-55-induced EAE as a valid model of MS via amelioration of pathogenic molecular mechanisms responsible for neuroinflammation and axonal damage.

S-allylcysteine Improves Blood Flow Recovery and Prevents Ischemic Injury by Augmenting Neovasculogenesis

Studies suggest that a low level of circulating human endothelial progenitor cells (EPCs) is a risk factor for ischemic injury and coronary artery disease (CAD). Consumption of S-allylcysteine (SAC) is known to prevent CAD. However, the protective effects of SAC on the ischemic injury are not yet clear. In this study, we examined whether SAC could improve blood flow recovery in ischemic tissues through EPC-mediated neovasculogenesis. The results demonstrate that SAC significantly enhances the neovasculogenesis of EPCs in vitro. The molecular mechanisms for SAC enhancement of neovasculogenesis include the activation of Akt/endothelial nitric oxide synthase signaling cascades. SAC increased the expression of c-kit, β-catenin, cyclin D1, and Cyclin-dependent kinase 4 (CDK4) proteins in EPCs. Daily intake of SAC at dosages of 0.2 and 2 mg/kg body weight significantly enhanced c-kit protein levels in vivo. We conclude that dietary consumption of SAC improves blood flow recovery and prevents ischemic injury by inducing neovasculogenesis in experimental models.

Dose-dependent S-allyl cysteine ameliorates multiple sclerosis disease-related pathology by reducing oxidative stress and biomarkers of dysbiosis in experimental autoimmune encephalomyelitis

Garlic is a component of the Mediterranean diet. S-allyl cysteine (SAC), the most common organosulphur present in garlic, possesses neuroprotective properties. This investigation was performed to evaluate the dose-dependent protective action of SAC on oxidative damage, inflammation and gut microbiota alterations biomarkers. Experimental autoimmune encephalomyelitis (EAE) as a model of multiple sclerosis (MS) was induced by the myelin oligodendrocyte glycoprotein (MOG), whose effects were quantified by examining the changes in: clinical score, lipid peroxidation products, carbonylated proteins, glutathione system, tumor necrosis factor alpha (TNFα), and lipopolysaccharide membrane bacteria (LPS). Our results reveal that MOG induces paralysis, oxidative damage and increases in LPS binding protein (LBP) and LPS levels. In this work, two doses of SAC were compared with two dose of N-acetyl cysteine (NAC). SAC was more effective than NAC and it prevented the harmful effects induced by MOG more effectively at the dose of 50mg/kg than that of 18mg/kg. Surprisingly, NAC increases LBP levels while SAC had not such negative effect. In conclusion the data show the ability of SAC to modify EAE evolution.

Aged and Unaged Garlic Exerts Differential Effects on Cellular Aging via Modulation of Tissue Degradative and Antioxidant Enzymes Activity – A Cell-Free in Vitro Study

The effects of aged and unaged garlic on cell aging processes via enzymatic and oxidative pathways were examined in this cell-free in vitro study. Aged and unaged garlic, quercetin, and S-allyl cysteine inhibited collagenase and elastase dose-dependently. Quercetin and unaged garlic showed stronger collagenase inhibition and weaker elastase inhibition than S-allyl cysteine and aged garlic. Quercetin and aged garlic scavenged radicals more effectively than unaged garlic and S-allyl cysteine. Superoxide dismutase activity was significantly augmented by quercetin and unaged garlic when compared to aged garlic and S-allyl cysteine. Aged garlic contained higher amounts of S-allyl cysteine, total flavonoid and polyphenols, and lower quercetin content when compared to unaged garlic. Aged and unaged garlic exerted different effects on cellular aging by modulating collagenase, elastase, and superoxide dismutase activities. The different effects can potentially be attributed to different organosulfur and phenolic compositions.

Aged and Unaged Garlic Exerts Differential Effects on Cellular Aging via Modulation of Tissue Degradative and Antioxidant Enzymes Activity – A Cell-Free in Vitro Study

The effects of aged and unaged garlic on cell aging processes via enzymatic and oxidative pathways were examined in this cell-free in vitro study. Aged and unaged garlic, quercetin, and S-allyl cysteine inhibited collagenase and elastase dose-dependently. Quercetin and unaged garlic showed stronger collagenase inhibition and weaker elastase inhibition than S-allyl cysteine and aged garlic. Quercetin and aged garlic scavenged radicals more effectively than unaged garlic and S-allyl cysteine. Superoxide dismutase activity was significantly augmented by quercetin and unaged garlic when compared to aged garlic and S-allyl cysteine. Aged garlic contained higher amounts of S-allyl cysteine, total flavonoid and polyphenols, and lower quercetin content when compared to unaged garlic. Aged and unaged garlic exerted different effects on cellular aging by modulating collagenase, elastase, and superoxide dismutase activities. The different effects can potentially be attributed to different organosulfur and phenolic compositions.