Antioxidant activity of allicin, an active principle in garlic

Prasad, Kailash; Laxdal, Victor A.; Yu, Ming Chih; Raney, Barbara L.

doi:10.1007/bf00928155

Cited by 228 publications

(147 citation statements)

References 17 publications

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“…Administration of allicin with CP showed a significant decrease in the level of TBARS compared to rats treated with CP alone, a result which agrees with other reported data that demonstrated apparent decrease in TBARS after administration of allicin (Prasad et al, 1995;Li et al, 2010). This activity may be due to the ability of allicin to scavenge hydroxyl and peroxyl radicals and superoxide anion (Kim et al, 2001) and modulating LP (Saravanan & Prakash, 2004).…”

Section: Discussionsupporting

confidence: 92%

Modulation of cyclophosphamide-induced early lung injury by allicin

Ashry

Gameil

Suddеk

2013

Pharmaceutical Biology

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Context: Cyclophosphamide (CP) causes lung injury in rats through its ability to generate free radicals with subsequent epithelial and endothelial cell damage. Objective: This study was conducted to assess whether allicin can ameliorate CP-induced early lung injury in rats. Materials and methods: Male Sprague Dawely rats were divided into four groups. Group I was the control group. Group II received allicin (50 mg/kg/d, p.o.) for 14 consecutive days. Group III was injected once with CP (150 mg/kg, i.p.). Group IV received allicin for seven consecutive days, before and after CP injection (150 mg/kg, i.p.). The parameters of study were serum biomarkers, lung tissue antioxidant profile and histopathological changes in lung tissue. Results: A single intraperitoneal injection of CP markedly altered the levels of several biomarkers in lung homogenates. Significant increases in lung content of lipid hydroperoxides were seen that paralleled the decreased levels of total reduced glutathione. Superoxide dismutase activity (SOD) was significantly increased. CP increased the level of serum biomarkers; total protein, lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-a). Pretreatment of rats daily with oral allicin seven days prior to and seven days after CP inject significantly inhibited the development of lung injury, prevented the alterations in lung and serum biomarkers associated with inflammatory reactions, with less lipid peroxidation (LP) and restoration of antioxidants. Moreover, allicin attenuated the secretion of proinflammatory cytokine, TNF-a expression in rat serum. In addition, allicin effectively blunted CP-induced histopathological changes in lung tissue. Discussion and conclusion: Our results suggest that allicin is efficient in blunting CP-induced pulmonary damage.

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Section: Discussionsupporting

confidence: 92%

Modulation of cyclophosphamide-induced early lung injury by allicin

Ashry

Gameil

Suddеk

2013

Pharmaceutical Biology

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“…A variety of biological effects of allicin are attributed both to its SH-modifying and antioxidant properties [8,9]. L L-cysteine of the antioxidant glutathione may also be a target of allicin [5,10].…”

Section: Introductionmentioning

confidence: 99%

Suppression of Mycobacterium tuberculosis induced reactive oxygen species (ROS) and TNF‐α mRNA expression in human monocytes by allicin

et al. 2006

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Chronic inflammation associated with tumor necrosis factor (TNF)-a and reactive oxygen species (ROS) is the hallmark of tuberculosis. Mycobacterium tuberculosis (MTB) directly stimulates human monocytes to secrete TNF-a. We show the augmented expression of TNF-a mRNA in MTB-infected monocytes by cellular activation and ROS was suppressed by allicin in a dose-dependent manner. Also, allicin enhanced the glutathione peroxidase activity, which correlated inversely with the downregulation of ROS and TNF-a in MTB-infected monocytes. Hence, allicin may prove to be a valuable natural antioxidant in combating tuberculosis.

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“…Several reports (25)(26)(27) have indicated that allicin is the predominant active component that is responsible for the majority of the biological activities of garlic, including attenuating ischemic injury, lowering blood pressure and antiarrhythmic effects (6,28,29). The chemical structure of allicin is CH 2 =CH-CH 2 -S(O)-S-CH 2 -CH=CH 2 , and it has been has been manufactured synthetically and produced worldwide (18).…”

Section: Discussionmentioning

confidence: 99%

Allicin inhibits transient outward potassium currents in mouse ventricular myocytes

Cao

Huang

Wang

2016

Experimental and Therapeutic Medicine

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Abstract. Allicin is the active constituent of garlic, a widely used spice and food. The remedial properties of garlic have also been extensively researched and it has been demonstrated that allicin is able to inhibit the transient outward potassium current (I to ) in atrial myocytes. However, the direct effect of allicin on I to in ventricular myocytes has yet to be elucidated. In the present study, the effects of allicin on I to in ventricular myocytes isolated from mice were investigated, using the whole-cell patch recording technique. The results revealed that I to current was not significantly suppressed by allicin in the low-dose group (10 µmol/l; P>0.05). However, I to was significantly inhibited by higher doses of allicin (30, 100 and 300 µmol/l; P<0.05 vs. control; n=6) in a concentration-dependent manner (IC 50 =41.6 µmol/l). In addition, a high concentration of allicin (≥100 µmol/l) was able to accelerate the voltage-dependent inactivation of I to in mouse ventricular myocytes. In conclusion, the present study revealed that allicin inhibited the I to in mouse ventricular myocytes, which may be the mechanism through which allicin exerts its antiarrhythmic effect.

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Antioxidant activity of allicin, an active principle in garlic

Cited by 228 publications

References 17 publications

Modulation of cyclophosphamide-induced early lung injury by allicin

Modulation of cyclophosphamide-induced early lung injury by allicin

Suppression of Mycobacterium tuberculosis induced reactive oxygen species (ROS) and TNF‐α mRNA expression in human monocytes by allicin

Allicin inhibits transient outward potassium currents in mouse ventricular myocytes

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