Chrysanthemum Indicum Extract Research Articles

Corrosion Inhibition of Carbon Steel in Hydrochloric Acid by Chrysanthemum Indicum Extract

Corrosion Inhibition of Carbon Steel in Hydrochloric Acid by Chrysanthemum Indicum Extract

Corrigendum to "The Protective Effect of Chrysanthemum indicum Extract against Ankylosing Spondylitis in Mouse Models".

[This corrects the article DOI: 10.1155/2017/8206281.].

The Protective Effect of Chrysanthemum indicum Extract against Ankylosing Spondylitis in Mouse Models.

In traditional Chinese and Korean homeopathic medicine, Chrysanthemum indicum Linné (Asteraceae) is a time-honored herb, prescribed for the resolution of symptoms associated with inflammatory and hypertensive conditions as well as those affecting the lungs and its associated structures. The goal of this work is to investigate the defensive role of Chrysanthemum indicum extract in fighting ankylosing spondylitis (AS) using mouse models, through which the manifestation and extent of the disease progression were measured with quantitative analysis of the intervertebral joints. Markers of inflammation as well as oxidative stress were also analysed. Western blot was used to quantify the levels of Nuclear Factor-κB (NF-κB) p65, Dickkopf-1 (DKK-1), and sclerostin (SOST). Consequently, the findings of this experiment demonstrated that AS in mice that were given Chrysanthemum indicum extract had lower level of TNF-α, IL-1β, and IL-6 (P < 0.05) and increased level of catalase (CAT), glutathione peroxidase (GSH-PX), and superoxide dismutase (SOD) (P < 0.05). The results also revealed that Chrysanthemum indicum supplemented with diet contributed to a decrease in Nuclear Factor-κB (NF-κB) p65 protein expression (P < 0.05) and higher levels of DKK-1 and SOST proteins (P < 0.05). Therefore, we concluded that the beneficial role of Chrysanthemum indicum in AS is manifested through downregulating oxidative stress, inhibiting inflammatory mediators and NF-κB, and increasing DKK-1 and SOST levels.

Development of an LC-MS/MS method for determining the pharmacokinetics of clonidine following oral administration of Zhenju antihypertensive compound.

Zhenju antihypertensive compound (ZJAHC) is a combined Chinese-Western medicine formula including clonidine (CLO), hydrochlorothiazide (HCT), rutin, Chrysanthemum indicum extract and pearl powder. Compared with CLO preparations, ZJAHC shows improved activities and decreased adverse effects. It is believed that the side effects of CLO are caused by its high peak plasma concentration. Hence, study of the influence of ZJAHC on the pharmacokinetic behaviors of clonidine seems essential. In present study, the plasma concentrations of CLO were determined with a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. The MS/MS transitions monitored for clonidine and internal standard were 230.2 → 213.1 and 152.2 → 110.2, respectively. The analyte was quantified in a single run within 3 min. The pharmacokinetic study showed that the area under the plasma concentration-time curve of CLO in ZJAHC (60 µg/kg CLO) was similar to that of CLO-HCT-high (120 µg/kg CLO) but the peak concentration was much lower than that in CLO-HCT-high. ZJAHC could enhance the bioavailability without greatly increasing peak concentration of clonidine. This comprehensive effect of enhancing the bioavailability and avoiding the high peak plasma concentration for CLO might mainly result from the co-contribution of Western medicine and traditional Chinese medicine (TCM), while the effect of TCM was stronger than that of Western medicine.

Dual Effect of Chrysanthemum indicum Extract to Stimulate Osteoblast Differentiation and Inhibit Osteoclast Formation and Resorption In Vitro

The risk of bone-related diseases increases due to the imbalance between bone resorption and bone formation by osteoclasts and osteoblasts, respectively. The goal in the development of antiosteoporotic treatments is an agent that will improve bone through simultaneous osteoblast stimulation and osteoclast inhibition without undesirable side effects. To achieve this goal, numerous studies have been performed to identify novel approaches using natural oriental herbs to treat bone metabolic diseases. In the present study, we investigated the effect of Chrysanthemum indicum extract (CIE) on the differentiation of osteoclastic and osteoblastic cells. CIE inhibited the formation of TRAP-positive mature osteoclasts and of filamentous-actin rings and disrupted the bone-resorbing activity of mature osteoclasts in a dose-dependent manner. CIE strongly inhibited Akt, GSK3β, and IκB phosphorylation in RANKL-stimulated bone marrow macrophages and did not show any effects on MAP kinases, including p38, ERK, and JNK. Interestingly, CIE also enhanced primary osteoblast differentiation via upregulation of the expression of alkaline phosphatase and the level of extracellular calcium concentrations during the early and terminal stages of differentiation, respectively. Our results revealed that CIE could have a potential therapeutic role in bone-related disorders through its dual effects on osteoclast and osteoblast differentiation.

Teratogenic Effect of Ace Inhibitor (Lisinopril) and Chrysanthemum Indicum(Guldaudi) on Head and Face Region of Mice Fetuses

Lisinopril an ACE inhibitor when administered to pregnant mice was found to be teratogenic. Chrysanthemum indicum extract was also administered to pregnant mice and compared with the teratogenic effect with those produced by lisinopril. Thirteen pregnantfemale mice were administered lisinopril orally in the dose of 2mg/100g and Guldaudi extract 50mg/100g body weight of mice. Lisinopril and Guldaudi were administered to pregnant mice daily from day zero of pregnancy. On day 18 mother mice was sacrificed and pups were collected. These, showed significant stunting in size (p<0.001) in both lisinopril and guldaudi groups. Exencephaly was found in 26.08% in lisinopril group; however hypoplasia of skull was present in Guldaudi group. Resorption (5%) was noticed only in Guldaudi group. The lisinopril in dose of 2mg/100g body weight tried was found to be teratogenic and dose of Guldaudi extract in the dose of 50mg/100g was also found teratogenic with less severity as compared to 2 mg dose of lisinopril. Oligohydramnios and hypoxia following lisinopril and Guldaudi administration was attributed to be the cause of these malformations.

Effects of Chrysanthemum indicum extract on proliferation and apoptosis of human hepatocellular carcinoma MHCC97H cells

Objective To investigate the effect of Chrysanthemum indicum extract(CIE)on proliferation and apoptosis of hepatocellular carcinoma(HCC)MHCC97H cells and explore its mechanism.Methods MHCC97H cells cultured in vitro,pretreatment MHCC97H cells with CIE 0.4,0.8,1.2 mg/ml and blank control group,proliferation of cells was measured by microculture tetrazolium(MTT).Cell apoptosis and mitochondrial membrane potential(MMP ΔΨm)were determined by flow cytometry.Cytochrome C,Caspase-9 and-3 expression was measured by Western blot.Results CIE significantly inhibited proliferation of MHCC97H cells in a dose-and time-dependent manner.Compared with control group,CIE0.4,0.8,1.2 mg/ml induced MHCC97H cell apoptosis,decreased MMP ΔΨm,and enhanced cytochrome C,Caspase-9 and-3 protein expressions,respectively(P＜0.05).Conclusion CIE can inhibit proliferation of MHCC97H cells,which might be associated with inducing cancer cell apoptosis.Mitochondrial pathway could be one that CIE induce cancer cell apoptosis. Key words: Carcinoma hepatocellular; Chrysanthemum indicum; Apoptosis; MHCC97H; Mitochondrial membrane potential

Anti-inflammatory activity of Chrysanthemum indicum extract in acute and chronic cutaneous inflammation

Aim of the study Although Chrysanthemum indicum Linné (Compositae) has long been used in traditional Korean, Chinese, Japanese medicine to treat various immune-related diseases the underlying mechanism(s) by which these effects are induced remains to be defined in vivo model system. We investigated the effects of 70% ethanolic extract from Chrysanthemum indicum Linné (CIE) on skin inflammation in mice. Materials and methods Production of pro-inflammatory cytokines (TNF-α and IL-1β), activation of myeloperoxidase, and histological assessment were examined in acute and chronic skin inflammation using 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear edema. Results CIE inhibited topical edema in the mouse ear, following administration at 200 mg/kg (i.p.), leading to substantial reductions in skin thickness and tissue weight, inflammatory cytokine production, neutrophil-mediated myeloperoxidase activity, and various histopathological indicators. Furthermore, CIE was effective at reducing inflammatory damage induced by chronic TPA exposure. Conclusions These results demonstrate that CIE is an effective anti-inflammatory agent in murine phorbol ester-induced dermatitis, and suggest that the extract may have therapeutic potential in a variety of immune-related cutaneous diseases.

Induction of apoptosis and cell cycle arrest in human HCC MHCC97H cells with Chrysanthemum indicum extract

To investigate the effects of Chrysanthemum indicum extract (CIE) on inhibition of proliferation and on apoptosis, and the underlying mechanisms, in a human hepatocellular carcinoma (HCC) MHCC97H cell line. Viable rat hepatocytes and human endothelial ECV304 cells were examined by trypan blue exclusion and MTT assay, respectively, as normal controls. The proliferation of MHCC97H cells was determined by MTT assay. The cellular morphology of MHCC97H cells was observed by phase contrast microscopy. Flow cytometry was performed to analyze cell apoptosis with annexin V/propidium iodide (PI), mitochondrial membrane potential with rhodamine 123 and cell cycle with PI in MHCC97H cells. Apoptotic proteins such as cytochrome C, caspase-9, caspase-3 and cell cycle proteins, including P21 and CDK4, were measured by Western blotting. CIE inhibited proliferation of MHCC97H cells in a time- and dose-dependent manner without cytotoxicity in rat hepatocytes and human endothelial cells. CIE induced apoptosis of MHCC97H cells in a concentration-dependent manner, as determined by flow cytometry. The apoptosis was accompanied by a decrease in mitochondrial membrane potential, release of cytochrome C and activation of caspase-9 and caspase-3. CIE arrested the cell cycle in the S phase by increasing P21 and decreasing CDK4 protein expression. CIE exerted a significant apoptotic effect through a mitochondrial pathway and arrested the cell cycle by regulation of cell cycle-related proteins in MHCC97H cells without an effect on normal cells. The cancer-specific selectivity shown in this study suggests that the plant extract could be a promising novel treatment for human cancer.