A review of the cardiovascular benefits and antioxidant properties of allicin

Cardiovascular disease (CVD) is a category of chronic noncommunicable diseases causing high global mortality and has been a heavy social burden in many countries. In the search of chemicals that arise from natural food source, allicin is one such ingredient from garlic that was discovered with the potential to provide beneficial effects to the cardiovascular system. From the pharmacokinetic studies, allicin is known to be hydrophobic and can be readily absorbed through the cell membrane without inducing any damage to the phospholipid bilayer and then rapidly metabolized to exert pharmacological effects that are important to the cardiovascular system. It was found to provide cardio-protective effects by inducing vasorelaxation and alleviating various pathological conditions of CVD, including cardiac hypertrophy, angiogenesis, platelet aggregation, hyperlipidemia and hyperglycemia. Allicin was also discovered to further protect the cardiovascular system by enhancing the antioxidant status by lowering the level of reactive oxygen species and stimulating the production of glutathione. Other pharmacological benefits such as anticancer and antimicrobial activities were also discussed. It is concluded that allicin can be potentially developed into a health product for the cardiovascular system

Emodin induces cytotoxic effect in human breast carcinoma MCF-7 cell through modulating the expression of apoptosis-related genes

Context: The poor prognostic outcome of breast cancer is largely due to its resistance to cancer therapies. Development of therapeutic agents that can inhibit growth and induce apoptosis in breast cancer cells can help solve the problem. Emodin is an active anthraquinone that has been reported to have diverse biological effects. Objective: In this study, the anticancer effects of emodin on growth inhibition, apoptosis induction and the expression of apoptosis-related genes in MCF-7 cells were investigated. Materials and Methods: Growth inhibition induced by emodin was investigated by the MTS assay and the colony formation assay; while emodin-induced apoptosis was determined by the COMET assay and DNA fragmentation detection. Emodin (35 μM)-induced alterations in the expression of apoptotic-related genes were detected by using real-time PCR. Results: Emodin had significant growth inhibitory effects on MCF-7 cells with IC50 = 7.22 µg/ml (∼30 μM). It also exerted a concentration-dependant inhibitory effect on the colony-forming ability of MCF-7 cells with IC50 = 7.60 µg/ml (∼30 µM). Hallmarks of apoptosis, such as single-strand DNA breakage and DNA fragmentation, were observed in emodin-treated MCF-7 cells. The gene expression of Fas ligand (FASL) was up-regulated (p \u3c 0.01) but those of MCL1, CCND1 and C-MYC were down-regulated (p \u3c 0.05) in emodin-treated MCF-7 cells. Discussion and Conclusion: This study indicated that emodin could induce growth inhibition and apoptosis in MCF-7 cells through the modulation of the expression of apoptosis-related genes. The growth inhibitory effects of emodin might involve both the intrinsic and the extrinsic apoptotic pathways and cell cycle arrest

Allicin protects rat cardiomyoblasts (H9c2 cells) from hydrogen peroxide-induced oxidative injury through inhibiting the generation of intracellular reactive oxygen species

Oxidative stress is considered an important factor that promotes cell death in response to a variety of pathophysiological conditions. This study investigated the antioxidant properties of allicin, the principle ingredient of garlic, on preventing oxidative stress-induced injury. The antioxidant capacities of allicin were measured by using 1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging assay and hydrogen peroxide (H2O2)-induced cell damage on H9c2 cardiomyoblasts. Allicin (0.3–10 μM) pre-incubation could concentration-dependently attenuate the intracellular reactive oxygen species (ROS) increase induced by H2O2 on H9c2 cells. It could also protect H9c2 cells against H2O2-induced cell damage. However, the DPPH free radical scavenging activity of allicin was shown to be low. Therefore, it is believed that the protective effect of allicin on H9c2 cells could inhibit intracellular ROS production instead of scavenging extracellular H2O2 or free radicals. For the observed protective effect on H9c2 cells, allicin might also be effective in reducing free radical-induced myocardial cell death in ischemic condition

A validated HPLC method with dual wavelength detection on chlorogenic acid and internal standard in plasma and its application in pharmacokinetic study in rats

A validated high performance liquid chromatographic (HPLC) method with dual wavelength detection was developed and applied to the determination of chlorogenic acid in rat plasma. Elution was performed on C18 column at 27°C with acetronitrile–water (0.2% phosphoric acid, pH = 2.0) at different proportions according to a time scheduled programme and pumped at a flow rate of 1.0 mL min−1. The eluent was detected at 325 nm for chlorogenic acid and 370 nm for the internal standard, kaempferol. The intra-day and inter-day precisions were better than 3.58% and 3.66%, respectively. The standard curve for chlorogenic acid was linear (r2 = 0.9993) in the concentration range of 0.1–15 μg mL−1. Accuracy in the measurement of samples ranged from 91.97 to 101.81%. The limit of detection and the limit of quantification for chlorogenic acid in plasma were 30 and 90 ng mL−1, respectively. This assay has been successfully applied in the pharmacokinetic study of chlorogenic acid through oral and intravenous administration in rats. It showed that the low bioavailability of chlorogenic acid and an intravenous administration route is a better dosage regimen. It is a simple and sensitive analytical method with good accuracy and reproducibility. The current method also demonstrated that an internal standard with different optimal UV absorbance from that of the analyte can also be used in an analytical method

Enhancement of in vitro and in vivo anticancer activities of polysaccharide peptide from Grifola frondosa by chemical modifications

Context: Grifola frondosa (Polyporaceae), maitake, is a widely consumed edible mushroom in some Asian countries. The fruit bodies and mycelia of maitake have shown different bioactive compounds with anticancer and other therapeutic properties. Objective: This study evaluated three chemically modified maitake polysaccharide-peptides’ (MPSP) adjuvant effect (in vivo) and anticancer activity (in vitro growth inhibitory effect) compared with crude MPSP from G. frondosa. Materials and Methods: We investigated the possibility of enhancing the adjuvant effect and anticancer effect of crude MPSP by using simple chemical modification methods to convert crude MPSP to phosphorylated, acetylated or esterified MPSPs. The adjuvant effect and growth inhibitory effect were evaluated by C6 cell inoculated rat model with cyclophosphamide (CPA) treatment and in vitro cell viability assay, respectively. Results: All four tested MPSPs showed significant adjuvant effect to CPA treatment on rats inoculated with C6 cancer cells. In addition, an obvious growth inhibitory effect was observed in C6 cancer cells but not in normal brain cells treated with various forms of MPSPs. Only phosphorylation could significantly (p \u3c 0.05) improve the adjuvant effect (in vivo) and growth inhibitory effect. A same rank order (phosphorylated MPSP \u3e esterified MPSP ≥ acetylated MPSP ≥ crude MPSP) of efficacy was observed in both the in vivo and in vitro assays. Discussion and Conclusion: This study showed chemical phosphorylation could markedly enhance both adjuvant effects and growth inhibitory effects. This study demonstrated the feasibility of enhancing the efficacy of MPSP by using a simple chemical modification method, and this provides a foundation for future study in this area

Chlorogenic acid exhibits cholesterol lowering and tatty liver attenuating properties by up-regulating the gene expression of PPAR-α in hypercholesterolemic rats induced with a high-cholesterol diet

Hypercholesterolemia is a major risk factor for the development of cardiovascular disease and nonalcoholic fatty liver disease. Natural compounds have been proved to be useful in lowering serum cholesterol to slow down the progression of cardiovascular disease and nonalcoholic fatty liver disease. In the present study, the hypocholesterolemic and hepatoprotective effects of the dietary consumption of chlorogenic acid were investigated by monitoring plasma lipid profile (total cholesterol, triglycerides, high-density lipoprotein and low-density lipoprotein) in Sprague–Dawley rats fed with a normal diet, a high-cholesterol diet or a high-cholesterol diet supplemented with chlorogenic acid (1 or 10 mg/kg/day p.o.) for 28 days. Chlorogenic acid markedly altered the increased plasma total cholesterol and low-density lipoprotein but decreased high-density lipoprotein induced by a hypercholesterolemic diet with a dose-dependent improvement on both atherogenic index and cardiac risk factor. Lipid depositions in liver were attenuated significantly in hypercholesterolemic animals supplemented with chlorogenic acid. It is postulated that hypocholesterolemic effect is the primary beneficial effect given by chlorogenic acid, which leads to other secondary beneficial effects such as atheroscleroprotective, cardioprotective and hepatoprotective functions. The hypocholesterolemic functions of chlorogenic acid are probably due to the increase in fatty acids unitization in liver via the up-regulation of peroxisome proliferation-activated receptor α mRNA

Allicin protects rat cardiomyoblasts (H9c2 cells) from hydrogen peroxide-induced oxidative injury through inhibiting the generation of intracellular reactive oxygen species

Oxidative stress is considered an important factor that promotes cell death in response to a variety of pathophysiological conditions. This study investigated the antioxidant properties of allicin, the principle ingredient of garlic, on preventing oxidative stress-induced injury. The antioxidant capacities of allicin were measured by using 1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging assay and hydrogen peroxide (H2O2)-induced cell damage on H9c2 cardiomyoblasts. Allicin (0.3–10 μM) pre-incubation could concentration-dependently attenuate the intracellular reactive oxygen species (ROS) increase induced by H2O2 on H9c2 cells. It could also protect H9c2 cells against H2O2-induced cell damage. However, the DPPH free radical scavenging activity of allicin was shown to be low. Therefore, it is believed that the protective effect of allicin on H9c2 cells could inhibit intracellular ROS production instead of scavenging extracellular H2O2 or free radicals. For the observed protective effect on H9c2 cells, allicin might also be effective in reducing free radical-induced myocardial cell death in ischemic condition

Enhancement of in vitro

Context: Grifola frondosa (Polyporaceae), maitake, is a widely consumed edible mushroom in some Asian countries. The fruit bodies and mycelia of maitake have shown different bioactive compounds with anticancer and other therapeutic properties. Objective: This study evaluated three chemically modified maitake polysaccharide-peptides’ (MPSP) adjuvant effect (in vivo) and anticancer activity (in vitro growth inhibitory effect) compared with crude MPSP from G. frondosa. Materials and Methods: We investigated the possibility of enhancing the adjuvant effect and anticancer effect of crude MPSP by using simple chemical modification methods to convert crude MPSP to phosphorylated, acetylated or esterified MPSPs. The adjuvant effect and growth inhibitory effect were evaluated by C6 cell inoculated rat model with cyclophosphamide (CPA) treatment and in vitro cell viability assay, respectively. Results: All four tested MPSPs showed significant adjuvant effect to CPA treatment on rats inoculated with C6 cancer cells. In addition, an obvious growth inhibitory effect was observed in C6 cancer cells but not in normal brain cells treated with various forms of MPSPs. Only phosphorylation could significantly (p \u3c 0.05) improve the adjuvant effect (in vivo) and growth inhibitory effect. A same rank order (phosphorylated MPSP \u3e esterified MPSP ≥ acetylated MPSP ≥ crude MPSP) of efficacy was observed in both the in vivo and in vitro assays. Discussion and Conclusion: This study showed chemical phosphorylation could markedly enhance both adjuvant effects and growth inhibitory effects. This study demonstrated the feasibility of enhancing the efficacy of MPSP by using a simple chemical modification method, and this provides a foundation for future study in this area

Emodin induces cytotoxic effect in human breast carcinoma MCF-7 cell through modulating the expression of apoptosis-related genes

Context: The poor prognostic outcome of breast cancer is largely due to its resistance to cancer therapies. Development of therapeutic agents that can inhibit growth and induce apoptosis in breast cancer cells can help solve the problem. Emodin is an active anthraquinone that has been reported to have diverse biological effects. Objective: In this study, the anticancer effects of emodin on growth inhibition, apoptosis induction and the expression of apoptosis-related genes in MCF-7 cells were investigated. Materials and Methods: Growth inhibition induced by emodin was investigated by the MTS assay and the colony formation assay; while emodin-induced apoptosis was determined by the COMET assay and DNA fragmentation detection. Emodin (35 μM)-induced alterations in the expression of apoptotic-related genes were detected by using real-time PCR. Results: Emodin had significant growth inhibitory effects on MCF-7 cells with IC50 = 7.22 µg/ml (∼30 μM). It also exerted a concentration-dependant inhibitory effect on the colony-forming ability of MCF-7 cells with IC50 = 7.60 µg/ml (∼30 µM). Hallmarks of apoptosis, such as single-strand DNA breakage and DNA fragmentation, were observed in emodin-treated MCF-7 cells. The gene expression of Fas ligand (FASL) was up-regulated (p \u3c 0.01) but those of MCL1, CCND1 and C-MYC were down-regulated (p \u3c 0.05) in emodin-treated MCF-7 cells. Discussion and Conclusion: This study indicated that emodin could induce growth inhibition and apoptosis in MCF-7 cells through the modulation of the expression of apoptosis-related genes. The growth inhibitory effects of emodin might involve both the intrinsic and the extrinsic apoptotic pathways and cell cycle arrest