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Jing Gung Chung - One of the best experts on this subject based on the ideXlab platform.
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antitumor effects of Emodin on ls1034 human colon cancer cells in vitro and in vivo roles of apoptotic cell death and ls1034 tumor xenografts model
Food and Chemical Toxicology, 2012Co-Authors: Yi Shih, Jaung Geng Lin, Shu Wen Weng, Jai Sing Yang, Jo-hua Chiang, Nou Ying Tang, Meng Wei Lin, Kuang Chi Lai, Jing Pin Lin, Jing Gung ChungAbstract:Emodin, an active natural anthraquinone derivative, is found in the roots and rhizomes of numerous Chinese medicinal herbs and exhibits anticancer effects on many types of human cancer cell lines. The aim of this study investigated that Emodin induced apoptosis of human colon cancer cells (LS1034) in vitro and inhibited tumor nude mice xenografts bearing LS1034 in vivo. In in vitro study, Emodin induced cell morphological changes, decreased the percentage of viability, induced G2/M phase arrest and increased ROS and Ca(2+) productions as well as loss of mitochondrial membrane potential (ΔΨ(m)) in LS1034 cells. Emodin-triggered apoptosis was also confirmed by DAPI staining and these effects are concentration-dependent. Western blot analysis indicated that the protein levels of cytochrome c, caspase-9 and the ratio of Bax/Bcl-2 were increased in LS1034 cells after Emodin exposure. Emodin induced the productions of ROS and Ca(2+) release, and altered anti- and pro-apoptotic proteins, leading to mitochondrial dysfunction and activations of caspase-9 and caspase-3 for causing cell apoptosis. In in vivo study, Emodin effectively suppressed tumor growth in tumor nude mice xenografts bearing LS1034. Overall, the potent in vitro and in vivo antitumor activities of Emodin suggest that it might be developed for treatment of colon cancer in the future.
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Emodin aloe Emodin and rhein inhibit migration and invasion in human tongue cancer scc 4 cells through the inhibition of gene expression of matrix metalloproteinase 9
International Journal of Oncology, 2010Co-Authors: Ya Yin Chen, Suyin Chiang, Jaung Geng Lin, Yi Shih, Ching Lung Liao, Shu Wen Weng, Tung Yuan Lai, Jing Gung ChungAbstract:Emodin, aloe-Emodin and rhein are major compounds in rhubarb (Rheum palmatum L.), used in Chinese herbal medicine, and found to have antitumor properties including cell cycle arrest and apoptosis in many human cancer cells. Our previous studies also showed that Emodin, aloe-Emodin and rhein induced apoptosis in human tongue cancer SCC-4 cells. However, the detail regarding Emodin, aloe-Emodin and rhein affecting migration and invasion in SCC-4 cells are not clear. In the present study, we investigated whether or not Emodin, aloe-Emodin and rhein inhibited migration and invasion of SCC-4 cells. Herein, we demonstrate that Emodin, aloe-Emodin and rhein inhibit the protein levels and activities of matrix metalloproteinase-2 (MMP-2) but did not affect gene expression of MMP-2, however, they inhibited the gene expression of MMP-9 and all also inhibited the migration and invasion of human tongue cancer SCC-4 cells. MMP-9 (gelatinase-B) plays an important role and is the most associated with tumor migration, invasion and metastasis in various human cancers. Results from zymography and Western blotting showed that Emodin, aloe-Emodin and rhein treatment decrease the levels of MMP-2, urokinase plasminogen activator (u-PA) in a concentration-dependent manner. The order of inhibition of associated protein levels and gene expression of migration and invasion in SCC-4 cells are Emodin >aloe-Emodin >rhein. Our results provide new insight into the mechanisms by which Emodin, aloe-Emodin and rhein inhibit tongue cancers. In conclusion, these findings suggest that molecular targeting of MMP-9 mRNA expression by Emodin, aloe-Emodin and rhein might be a useful strategy for chemo-prevention and/or chemo-therapeutics of tongue cancers.
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Emodin aloe Emodin and rhein induced dna damage and inhibited dna repair gene expression in scc 4 human tongue cancer cells
Anticancer Research, 2010Co-Authors: Ya Yin Chen, Suyin Chiang, Jaung Geng Lin, Ching Lung Liao, Tung Yuan Lai, Jai Sing Yang, Nou Ying Tang, Jing Gung ChungAbstract:In our primary studies, we have shown that Emodin, aloe-Emodin and rhein induced cytotoxic effects, including cell cycle arrest and apoptosis in SCC-4 human tongue cancer cells. However, details regarding their effects on DNA damage and repair gene expression in SCC-4 cells are not clear. We investigated whether or not Emodin, aloe-Emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 cells. Comet assay (single cell electrophoresis) indicated that incubation of SCC-4 cells with 0, 20, 30 and 40 microM of Emodin, 0, 25, 50 and 100 microM of aloe-Emodin or rhein led to a longer DNA migration smear (comet tail). This means that all examined agents induced DNA damage in SCC-4 cells and these effects are dose-dependent but Emodin is stronger than that of aloe-Emodin or rhein. The results from real-time PCR assay demonstrated that 30 microM of Emodin or aloe-Emodin used for 24 and 48 h treatment in SCC-4 cells significantly inhibited expression of genes associated with DNA damage and repair [ataxia telangiectasia mutated (ATM); ataxia-telangiectasia and Rad3-related (ATR); 14-3-3sigma (14-3-3sigma); breast cancer 1, early onset (BRCA1); and DNA-dependent serine/threonine protein kinase (DNA-PK)]; only rhein suppressed the expression of O(6)-methylguanine-DNA methyltransferase (MGMT) mRNA with 48 h treatment, but had no effect on ATM expression. On 24 h treatment, only aloe-Emodin significantly affected ATM expression. These effects may be the vital factors for Emodin, aloe-Emodin and rhein induction of DNA damage in vitro. In conclusion, these agents induced DNA damage followed by the inhibition of DNA repair-associated gene expressions, including ATM, ATR, 14-3-3sigma, BRCA1, DNA-PK and MGMT in SCC-4 human tongue cancer cells.
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Emodin aloe Emodin and rhein induced dna damage and inhibited dna repair gene expression in scc 4 human tongue cancer cells
Anticancer Research, 2010Co-Authors: Ya Yin Chen, Suyin Chiang, Jaung Geng Lin, Ching Lung Liao, Tung Yuan Lai, Jai Sing Yang, Nou Ying Tang, Jing Gung ChungAbstract:In our primary studies, we have shown that Emodin, aloe-Emodin and rhein induced cytotoxic effects, including cell cycle arrest and apoptosis in SCC-4 human tongue cancer cells. However, details regarding their effects on DNA damage and repair gene expression in SCC-4 cells are not clear. We investigated whether or not Emodin, aloe- Emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 cells. Comet assay (single cell electrophoresis) indicated that incubation of SCC-4 cells with 0, 20, 30 and 40 μM of Emodin, 0, 25, 50 and 100 μM of aloe-Emodin or rhein led to a longer DNA migration smear (comet tail). This means that all examined agents induced DNA damage in SCC-4 cells and these effects are dose-dependent but Emodin is stronger than that of aloe- Emodin or rhein. The results from real-time PCR assay demonstrated that 30 μM of Emodin or aloe-Emodin used for 24 and 48 h treatment in SCC-4 cells significantly inhibited expression of genes associated with DNA damage and repair (ataxia telangiectasia mutated (ATM); ataxia-telangiectasia and Rad3-related (ATR); 14-3-3sigma (14-3-3σ); breast cancer 1, early onset (BRCA1); and DNA-dependent serine/threonine protein kinase (DNA-PK)); only rhein suppressed the expression of O 6 -methylguanine-DNA
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aloe Emodin induces cell death through s phase arrest and caspase dependent pathways in human tongue squamous cancer scc 4 cells
Anticancer Research, 2009Co-Authors: Tsan Hung Chiu, Te Chun Hsia, Jai Sing Yang, Ping Ping Wu, Chia Yu, Chin Chin Ho, Hsu Feng Lu, Gibson W Wood, Jing Gung ChungAbstract:Aloe-Emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of aloe-Emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that aloe-Emodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 μM of aloe-Emodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. Aloe-Emodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (ΔΨ m ) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N- acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-Emodin-induced apoptosis. Aloe-Emodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. Aloe-Emodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.
Guang Shan - One of the best experts on this subject based on the ideXlab platform.
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Emodin an anthraquinone derivative from rheum officinale baill enhances cutaneous wound healing in rats
European Journal of Pharmacology, 2007Co-Authors: Tian Tang, Longwu Yin, Jing Yang, Guang ShanAbstract:Emodin (1, 3, 8-trihydroxy-6-methyl-anthraquinone) is an anthraquinone derivative from the roots of Rheum officinale Baill, a Chinese herb widely and traditionally used for wound healing. Our objective was to determine whether topically applied Emodin enhanced repair of rats' excisional wounds and its possible mechanism. Wounds were treated with either topical Emodin (100, 200 and 400 microg/ml), recombinant human epidermal growth factor (rhEGF, 10 microg/ml), or vehicle for 7 or 14 days consecutively. At day 5 postinjury, wounds receiving Emodin (400 microg/ml) were significantly smaller than those treated with vehicle. Emodin treatments had markedly more hydroxyproline content in day 7 wounds and tensile strength in day 14 wounds than that of vehicle control. The level of transforming growth factor- beta(1) (TGF-beta(1)) in wound tissues assessed by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR), showed a dose-dependent increase in Emodin-treated wounds compared with vehicle. Western immunoblotting analysis of wound tissues for Smad 2, 3, 4, 7 protein expression showed increase in Smad 2, 3 in the Emodin-treated wounds compared with vehicle. In contrast, a reduction of Smad 7 was observed in Emodin-treated wounds compared with vehicle and no change of Smad 4. In summary, our results showed that Emodin promoted repair of rats' excisional wounds via a complex mechanism involving stimulation of tissue regeneration and regulating Smads-mediated TGF-beta(1) signaling pathway.
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Emodin, an anthraquinone derivative from Rheum officinale Baill, enhances cutaneous wound healing in rats
European journal of pharmacology, 2007Co-Authors: Tian Tang, Longwu Yin, Jing Yang, Guang ShanAbstract:Abstract Emodin (1, 3, 8-trihydroxy-6-methyl-anthraquinone) is an anthraquinone derivative from the roots of Rheum officinale Baill, a Chinese herb widely and traditionally used for wound healing. Our objective was to determine whether topically applied Emodin enhanced repair of rats' excisional wounds and its possible mechanism. Wounds were treated with either topical Emodin (100, 200 and 400 μg/ml), recombinant human epidermal growth factor (rhEGF, 10 μg/ml), or vehicle for 7 or 14 days consecutively. At day 5 postinjury, wounds receiving Emodin (400 μg/ml) were significantly smaller than those treated with vehicle. Emodin treatments had markedly more hydroxyproline content in day 7 wounds and tensile strength in day14 wounds than that of vehicle control. The level of transforming growth factor- β 1 (TGF-β 1 ) in wound tissues assessed by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR), showed a dose-dependent increase in Emodin-treated wounds compared with vehicle. Western immunoblotting analysis of wound tissues for Smad 2, 3, 4, 7 protein expression showed increase in Smad 2, 3 in the Emodin-treated wounds compared with vehicle. In contrast, a reduction of Smad 7 was observed in Emodin-treated wounds compared with vehicle and no change of Smad 4. In summary, our results showed that Emodin promoted repair of rats' excisional wounds via a complex mechanism involving stimulation of tissue regeneration and regulating Smads-mediated TGF-β 1 signaling pathway.
Jai Sing Yang - One of the best experts on this subject based on the ideXlab platform.
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antitumor effects of Emodin on ls1034 human colon cancer cells in vitro and in vivo roles of apoptotic cell death and ls1034 tumor xenografts model
Food and Chemical Toxicology, 2012Co-Authors: Yi Shih, Jaung Geng Lin, Shu Wen Weng, Jai Sing Yang, Jo-hua Chiang, Nou Ying Tang, Meng Wei Lin, Kuang Chi Lai, Jing Pin Lin, Jing Gung ChungAbstract:Emodin, an active natural anthraquinone derivative, is found in the roots and rhizomes of numerous Chinese medicinal herbs and exhibits anticancer effects on many types of human cancer cell lines. The aim of this study investigated that Emodin induced apoptosis of human colon cancer cells (LS1034) in vitro and inhibited tumor nude mice xenografts bearing LS1034 in vivo. In in vitro study, Emodin induced cell morphological changes, decreased the percentage of viability, induced G2/M phase arrest and increased ROS and Ca(2+) productions as well as loss of mitochondrial membrane potential (ΔΨ(m)) in LS1034 cells. Emodin-triggered apoptosis was also confirmed by DAPI staining and these effects are concentration-dependent. Western blot analysis indicated that the protein levels of cytochrome c, caspase-9 and the ratio of Bax/Bcl-2 were increased in LS1034 cells after Emodin exposure. Emodin induced the productions of ROS and Ca(2+) release, and altered anti- and pro-apoptotic proteins, leading to mitochondrial dysfunction and activations of caspase-9 and caspase-3 for causing cell apoptosis. In in vivo study, Emodin effectively suppressed tumor growth in tumor nude mice xenografts bearing LS1034. Overall, the potent in vitro and in vivo antitumor activities of Emodin suggest that it might be developed for treatment of colon cancer in the future.
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Emodin Induces Apoptotic Death in Murine Myelomonocytic Leukemia WEHI-3 Cells In Vitro and Enhances Phagocytosis in Leukemia Mice In Vivo
Hindawi Limited, 2011Co-Authors: Yuan-chang Chang, Tung Yuan Lai, Jai Sing Yang, Hung-yi Chen, Fu-shin Chueh, Jo-hua Chiang, Wen-wen HuangAbstract:Emodin is one of major compounds in rhubarb (Rheum palmatum L.), a plant used as herbal medicine in Chinese population. Although many reports have shown that Emodin exhibits anticancer activity in many tumor cell types, there is no available information addressing Emodin-affected apoptotic responses in the murine leukemia cell line (WEHI-3) and modulation of the immune response in leukemia mice. We investigated that Emodin induced cytotoxic effects in vitro and affected WEHI-3 cells in vivo. This study showed that Emodin decreased viability and induced DNA fragmentation in WEHI-3 cells. Cells after exposure to Emodin for 24 h have shown chromatin condensation and DNA damage. Emodin stimulated the productions of ROS and Ca2+ and reduced the level of ΔΨm by flow cytometry. Our results from Western blotting suggest that Emodin triggered apoptosis of WEHI-3 cells through the endoplasmic reticulum (ER) stress, caspase cascade-dependent and -independent mitochondrial pathways. In in vivo study, Emodin enhanced the levels of B cells and monocytes, and it also reduced the weights of liver and spleen compared with leukemia mice. Emodin promoted phagocytic activity by monocytes and macrophages in comparison to the leukemia mice group. In conclusions, Emodin induced apoptotic death in murine leukemia WEHI-3 cells and enhanced phagocytosis in the leukemia animal model
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Emodin aloe Emodin and rhein induced dna damage and inhibited dna repair gene expression in scc 4 human tongue cancer cells
Anticancer Research, 2010Co-Authors: Ya Yin Chen, Suyin Chiang, Jaung Geng Lin, Ching Lung Liao, Tung Yuan Lai, Jai Sing Yang, Nou Ying Tang, Jing Gung ChungAbstract:In our primary studies, we have shown that Emodin, aloe-Emodin and rhein induced cytotoxic effects, including cell cycle arrest and apoptosis in SCC-4 human tongue cancer cells. However, details regarding their effects on DNA damage and repair gene expression in SCC-4 cells are not clear. We investigated whether or not Emodin, aloe-Emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 cells. Comet assay (single cell electrophoresis) indicated that incubation of SCC-4 cells with 0, 20, 30 and 40 microM of Emodin, 0, 25, 50 and 100 microM of aloe-Emodin or rhein led to a longer DNA migration smear (comet tail). This means that all examined agents induced DNA damage in SCC-4 cells and these effects are dose-dependent but Emodin is stronger than that of aloe-Emodin or rhein. The results from real-time PCR assay demonstrated that 30 microM of Emodin or aloe-Emodin used for 24 and 48 h treatment in SCC-4 cells significantly inhibited expression of genes associated with DNA damage and repair [ataxia telangiectasia mutated (ATM); ataxia-telangiectasia and Rad3-related (ATR); 14-3-3sigma (14-3-3sigma); breast cancer 1, early onset (BRCA1); and DNA-dependent serine/threonine protein kinase (DNA-PK)]; only rhein suppressed the expression of O(6)-methylguanine-DNA methyltransferase (MGMT) mRNA with 48 h treatment, but had no effect on ATM expression. On 24 h treatment, only aloe-Emodin significantly affected ATM expression. These effects may be the vital factors for Emodin, aloe-Emodin and rhein induction of DNA damage in vitro. In conclusion, these agents induced DNA damage followed by the inhibition of DNA repair-associated gene expressions, including ATM, ATR, 14-3-3sigma, BRCA1, DNA-PK and MGMT in SCC-4 human tongue cancer cells.
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Emodin aloe Emodin and rhein induced dna damage and inhibited dna repair gene expression in scc 4 human tongue cancer cells
Anticancer Research, 2010Co-Authors: Ya Yin Chen, Suyin Chiang, Jaung Geng Lin, Ching Lung Liao, Tung Yuan Lai, Jai Sing Yang, Nou Ying Tang, Jing Gung ChungAbstract:In our primary studies, we have shown that Emodin, aloe-Emodin and rhein induced cytotoxic effects, including cell cycle arrest and apoptosis in SCC-4 human tongue cancer cells. However, details regarding their effects on DNA damage and repair gene expression in SCC-4 cells are not clear. We investigated whether or not Emodin, aloe- Emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 cells. Comet assay (single cell electrophoresis) indicated that incubation of SCC-4 cells with 0, 20, 30 and 40 μM of Emodin, 0, 25, 50 and 100 μM of aloe-Emodin or rhein led to a longer DNA migration smear (comet tail). This means that all examined agents induced DNA damage in SCC-4 cells and these effects are dose-dependent but Emodin is stronger than that of aloe- Emodin or rhein. The results from real-time PCR assay demonstrated that 30 μM of Emodin or aloe-Emodin used for 24 and 48 h treatment in SCC-4 cells significantly inhibited expression of genes associated with DNA damage and repair (ataxia telangiectasia mutated (ATM); ataxia-telangiectasia and Rad3-related (ATR); 14-3-3sigma (14-3-3σ); breast cancer 1, early onset (BRCA1); and DNA-dependent serine/threonine protein kinase (DNA-PK)); only rhein suppressed the expression of O 6 -methylguanine-DNA
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aloe Emodin induces cell death through s phase arrest and caspase dependent pathways in human tongue squamous cancer scc 4 cells
Anticancer Research, 2009Co-Authors: Tsan Hung Chiu, Te Chun Hsia, Jai Sing Yang, Ping Ping Wu, Chia Yu, Chin Chin Ho, Hsu Feng Lu, Gibson W Wood, Jing Gung ChungAbstract:Aloe-Emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of aloe-Emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that aloe-Emodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 μM of aloe-Emodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. Aloe-Emodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (ΔΨ m ) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N- acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-Emodin-induced apoptosis. Aloe-Emodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. Aloe-Emodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.
Hong Xia - One of the best experts on this subject based on the ideXlab platform.
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Emodin inhibits voltage dependent potassium current in guinea pig gallbladder smooth muscle
Basic & Clinical Pharmacology & Toxicology, 2009Co-Authors: Hong XiaAbstract:Emodin is known to prompt bile secretion in gallbladder and to be used in the treatment of cholesterol stones. We studied the effects of Emodin on the contraction of gallbladder smooth muscle and voltage-dependent K(+) current in gallbladder smooth muscle cells. Gallbladder muscle strips were obtained from adult guinea pigs and the resting tension was recorded. Gallbladder smooth muscle cells were isolated by enzymatic digestion, and K(+) current was recorded by the whole-cell patch clamp method. Emodin increased the resting tension of gallbladder smooth muscle strips and inhibited voltage-dependent K(+) current in a dose-dependent manner. When 10 microM Emodin was applied to gallbladder smooth muscle cells for 3-6 min., the amplitude of voltage-dependent K(+) current was decreased by 31.5 +/- 0.5% at +40 mV, and this inhibitory effect mostly recovered after washout. The steady-state inactivation curves were shifted in a hyperpolarizing direction by Emodin. In the presence of the protein kinase C inhibitors staurosporine and chelerythrine, the effect of Emodin on voltage-dependent K(+ )current was significantly attenuated. In conclusion, Emodin promotes gallbladder contraction, mainly by inhibiting voltage-dependent K(+) current via the protein kinase C pathway. These findings provide theoretical foundation for the application of Emodin in gallbladder motility disorders.
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Emodin increases ca2 influx through l type ca2 channel in guinea pig gallbladder smooth muscle
European Journal of Pharmacology, 2008Co-Authors: Hong XiaAbstract:Abstract Emodin is known to be used in the treatment of cholesterol stones and cholecystitis. This study sought to investigate the effects of Emodin on the contraction of gallbladder smooth muscle (GBSM), intracellular Ca 2+ concentration and L-type calcium current in GBSM cells. Gallbladder muscle strips were obtained from adult guinea pigs and the resting tension was recorded. Gallbladder smooth muscle cells were isolated by enzymatic digestion. Cells were loaded with fluo-3/AM and [Ca 2+ ] i was determined by a laser confocal microscope. Calcium current was recorded by the whole-cell patch clamp method. Emodin increased the resting tension of GBSM strips in a dose-dependent manner. Emodin elevated [Ca 2+ ] i in GBSM cells, and this effect was attenuated by pretreatment with nifedipine. In addition, Emodin increased L-type calcium current at concentrations of 1 to 30 µM (at + 10 mV, 10 µM, 45.1 ± 5.2% compared to control, EC 50 = 3.11 µM). In the presence of protein kinase C (PKC) inhibitor, Staurosporine, Emodin did not significantly affect the calcium current. However, phorbol 12, 13-dibutyrate mimicked Emodin in enhancement of the calcium current. These results suggest that Emodin promotes gallbladder contraction by increasing Ca 2+ influx through L-type calcium channel via PKC pathway.
Tian Tang - One of the best experts on this subject based on the ideXlab platform.
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Emodin an anthraquinone derivative from rheum officinale baill enhances cutaneous wound healing in rats
European Journal of Pharmacology, 2007Co-Authors: Tian Tang, Longwu Yin, Jing Yang, Guang ShanAbstract:Emodin (1, 3, 8-trihydroxy-6-methyl-anthraquinone) is an anthraquinone derivative from the roots of Rheum officinale Baill, a Chinese herb widely and traditionally used for wound healing. Our objective was to determine whether topically applied Emodin enhanced repair of rats' excisional wounds and its possible mechanism. Wounds were treated with either topical Emodin (100, 200 and 400 microg/ml), recombinant human epidermal growth factor (rhEGF, 10 microg/ml), or vehicle for 7 or 14 days consecutively. At day 5 postinjury, wounds receiving Emodin (400 microg/ml) were significantly smaller than those treated with vehicle. Emodin treatments had markedly more hydroxyproline content in day 7 wounds and tensile strength in day 14 wounds than that of vehicle control. The level of transforming growth factor- beta(1) (TGF-beta(1)) in wound tissues assessed by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR), showed a dose-dependent increase in Emodin-treated wounds compared with vehicle. Western immunoblotting analysis of wound tissues for Smad 2, 3, 4, 7 protein expression showed increase in Smad 2, 3 in the Emodin-treated wounds compared with vehicle. In contrast, a reduction of Smad 7 was observed in Emodin-treated wounds compared with vehicle and no change of Smad 4. In summary, our results showed that Emodin promoted repair of rats' excisional wounds via a complex mechanism involving stimulation of tissue regeneration and regulating Smads-mediated TGF-beta(1) signaling pathway.
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Emodin, an anthraquinone derivative from Rheum officinale Baill, enhances cutaneous wound healing in rats
European journal of pharmacology, 2007Co-Authors: Tian Tang, Longwu Yin, Jing Yang, Guang ShanAbstract:Abstract Emodin (1, 3, 8-trihydroxy-6-methyl-anthraquinone) is an anthraquinone derivative from the roots of Rheum officinale Baill, a Chinese herb widely and traditionally used for wound healing. Our objective was to determine whether topically applied Emodin enhanced repair of rats' excisional wounds and its possible mechanism. Wounds were treated with either topical Emodin (100, 200 and 400 μg/ml), recombinant human epidermal growth factor (rhEGF, 10 μg/ml), or vehicle for 7 or 14 days consecutively. At day 5 postinjury, wounds receiving Emodin (400 μg/ml) were significantly smaller than those treated with vehicle. Emodin treatments had markedly more hydroxyproline content in day 7 wounds and tensile strength in day14 wounds than that of vehicle control. The level of transforming growth factor- β 1 (TGF-β 1 ) in wound tissues assessed by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR), showed a dose-dependent increase in Emodin-treated wounds compared with vehicle. Western immunoblotting analysis of wound tissues for Smad 2, 3, 4, 7 protein expression showed increase in Smad 2, 3 in the Emodin-treated wounds compared with vehicle. In contrast, a reduction of Smad 7 was observed in Emodin-treated wounds compared with vehicle and no change of Smad 4. In summary, our results showed that Emodin promoted repair of rats' excisional wounds via a complex mechanism involving stimulation of tissue regeneration and regulating Smads-mediated TGF-β 1 signaling pathway.