They could be formed either with the cyclization of linear octa-[40], [41],[32],and[42]22-(Hydroxymethyl)-AQH HOCH2 HHHHHH [43] and??[44]32-Methoxy-AQH MeO HHHHHH [42]42-Hydroxy-AQH OH HHHHHH [42]51-Methoxy-AQOH H HHHHHH [45, 46]61-Hydroxy-2-methyl AQOH Me personally HHHHHH [42][46][39][39][39], [39], andRubia yunnanensis[43]71-Hydroxy-2-(hydroxymethyl)-AQOH HOCH2 HHHHHH [32]82-(Ethoxycarbonyl)-1-hydroxy-AQOH EtOOC HHHHHH [39]91-Methoxy-2-methyl-AQMeO Me personally HHHHHH [39],[39], and[47]11Alizarin 2-methyl ether[42][39],[32], and [47]12Alizarin 1-methyl ether[42]13Alizarin 1,2-dimethyldiether[42]14Rubiadin (1,3-dihydroxy-2-[40][42][32], and[39],Rubia yunnanensis[43]15Lucidin (1,3-dihydroxy-2-[32][42], and[33]16Nordamnacanthal (1,3-dihydroxy-2-formyl-AQ)OHCHOOHHHHHH [32] and Rubia iberica[33] 17Munjistin (1,3-dihydroxy-2-carboxy-AQ)OHHOOCOHHHHHH [42]181,3-Dihydroxy-2-(methoxycarbonyl)-AQOHMeOOCOHHHHHH [32]192-(Ethoxymethyl)-1,3-dihydroxy-AQOHEtOCH2 OHHHHHH [32]201,3-Dihydroxy-2-(methoxymethyl)-AQOHMeOCH2 OHHHHHH [32] 21Lucidin dimethyl etherMeOHHOCH2 MeOHHHHH [39]22Munjistin dimethyl ether (2-carboxy-[32]232-BenzylxanthopurpurinOHPhCH2 OHHHHHH [32]24Anthragallol 3-methyl etherOHOHMeOHHHHH [42]25Anthragallol 2,3-dimethyl etherOHMeOMeOHHHHH [32] 262-Carboxy-1-hydroxy-3-methoxy-AQOHHOOCMeOHHHHH [48]273-Hydroxy-1-methoxy-2-(methoxymethyl)-AQMeOMeOCH2 OHHHHHH [49]28Anthragallol (1,2,3-trihydroxy-AQ)OHOHOHHHHHH [32]29Purpurin (1,2,4-trihydroxy AQ)OHOHHOHHHHH [32, 42][32][33][33], andRubia tetragona[32]30Quinizarin (1,4-dihydroxy-AQ)OHHHOHHHHH [32] andRubia tinctorum[32]311,4-Dihydroxy-2-(hydroxymethyl)-AQOHHOCH2 HOHHHHH [32] andRubia yunnanensis[32]322-(Ethoxycarbonyl)-1,4-dihydroxy-AQOHEtOOCHOHHHHH [32]33Christophine (2-(ethoxymethyl)-[32]341,4-Dihydroxy-2-methyl-AQOHMeHOHHHHH [32] and [32]35Xanthopurpurin (1,3-dihydroxy-AQ)OHHOHHHHHH [32][32][39][43],36Xanthopurpurin 3-methyl ether[32]37Xanthopurpurin dimethyl ether (1,3-dimethoxy-AQ)MeOHMeOHHHHH [32] 381-Hydroxy-3-(methoxycarbonyl)-AQOHHMeOOCHHHHH [32], [39], and [39]39Pseudopurpurin (3-(carboxy)-1,2,4-trihydroxy-AQ)OHOHHOOCOHHHHH [32][32][32]401,4-Dihydroxy-2-methyl-5-methoxy-AQOHMeHOHMeOHHH [50]411,4-Dihydroxy-2-methyl-8-methoxy-AQOHMeHOHHHHMeO [50]421,4-Dihydroxy-6-methyl-AQOHHHOHHMeHH [51]431,5-Dihydroxy-2-methyl-AQOHMeHHOHHHH [51]44Physcion (1,8-dihydroxy-3-methoxy-6-methyl-AQ)OHHMeHHMeHOH [50] and[52]452-Methyl-1,3,6-trihydroxy-AQOHMeOHHHOHHH [32][32][43], [32], and[32]461,4-Dihydroxy-7-methyl-AQOHHHOHHHMeH [50]474,5-Dihydroxy-2-methoxy-7-methyl-AQHMeHOHOHHMeOH [50]482,7-Dihydroxy-4-methoxy-3-methyl-AQHOHMeMeOHHOHH [32]492-Hydroxy-7-methyl-AQHMeHHHHOHH [32]502-Carboxy-4-hydroxy-AQHHOOCHOHHHHH [32] 51 3-([32]523-(6-O-Acetyl-[32] 533-[(2-O-6-Deoxy-[32], [32][39],[43] 543-[(3-O-Acetyl-2-O-6-deoxy-[32]553-[(6-O-Acetyl-2-O-6-deoxy-[32][39],[43][32]563-[(3,6-O-Diacetyl-2-O-6-deoxy-[32]573-[(4,6-O-Diacetyl-2-O-6-deoxy-[32]583-[(4-O-Acetyl-2-O-6-deoxy-[32]593-[(6-O-Acetyl-2-O-[32]60Ruberythric acidity (1-hydroxy-2-[(6-O-[32][32], and?[45]61Lucidin primeveroside (1-hydroxy-2-(hydroxymethyl)-3-[(6-O-[32][32][45], and [32] 632-[(6-O-[32] and[32]643-[(2-O-6-Deoxy-[32]653-([32]663-([32] 672-([32]683-([32]69Emodin (1,3,8-trihydroxy-6-methyl-AQ)OHHMeHHOHHOH [28, 52]70Cascarin (emodin 6-O-rhamnoside)OHHMeHHRhaOHOH [28]73Aloe-emodin (1,8-dihydroxy 3-hydroxy methyl anthraquinone)OHHCH2OHHHHHOH [53], [53], andRheum rhaponticum[53]74Chrysophanol (1,8-dihydroxy-3-methyl-AQ)OHHMeHHMeOHOH Fallopia japonicaF. with an focus on latest results about their immune system regulation. We talk about the experience and framework romantic relationship, mode of actions, and healing potential from the anthraquinones in autoimmune diabetes, including a fresh strategy for the usage of the anthraquinones in autoimmune diabetes. 1. Autoimmune Diabetes 1.1. Etiology and Therapies for Autoimmune Diabetes Autoimmune diabetes (Help) is normally a life-threatening metabolic disease that’s initiated and advances through a complicated interplay of environmental, hereditary, and immune elements. As a total result, insulin-producing subunit to guanosine triphosphate as well as the dissociation from the Gsubunit in the Gsubunit. This activates proteins tyrosine kinases, mitogen-activated proteins (MAP) kinases, and phospholipase C. Supplementary messengers, inositol diacylglycerol and triphosphate, which are transformed from phosphatidylinositol by phospholipase C, induce mobile calcium mineral translocation/activation and influx of proteins kinase C, respectively. The above mentioned biochemical cascades result in cell chemotaxis and various other cell features (Amount 4(a)) [16]. Therefore, chemokines/chemokine receptors have already been proposed as medication goals for inflammatory illnesses [14, 17C19]. For example, the initial FDA accepted CXCR4 antagonist, plerixafor/AMD3100, can be used to mobilize hematopoietic stem cells, that are gathered for make use of in stem cell graft in sufferers with hematological malignancies. Plerixafor was developed to hinder SDF-1/CXCR4 connections and shows guarantee for HIV an infection, malignancies, and autoimmune diseases such as rheumatoid arthritis [20]. However, this drug is usually expensive because of the difficulty in its total synthesis. There is, therefore, a demand for the discovery of new CXCR4 Rabbit polyclonal to ZBTB8OS antagonists that are both cost-effective and potent. Open in a separate window Physique 2 Chemokines and their cognate receptors. Twenty-three chemokine receptors and their natural ligands are classified into CCR, CXCR, and other categories. Open in a separate window Physique 4 Mode of action of catenarin and other anthraquinones for AID. (a) Upon chemokine binding, a chemokine receptor is usually activated and induces G protein activation. A cascade of calcium mobilization and activation/phosphorylation of MAPKK/MAPK pathways prospects to chemotaxis of leukocytes and, subsequently, insulitis and diabetes. (b) Catenarin and probably other anthraquinones inhibit leukocyte migration mediated by CCR5 and CXCR4 via the inactivation of MAPKs (p38 and JNK), MKKs (MKK6 and MKK7), and calcium mobilization. As a result, anthraquinones can suppress insulitis and diabetes. Since T cells and other leukocytes are thought to be essential players in AID [3, 21], interference with chemokine receptors in leukocytes could be a encouraging approach for treating insulitis and AID prophylaxis. CXCR4 is usually expressed in all the leukocytes including na?ve T cells [22]. CCR5 is usually preferentially expressed in activated T cells and macrophages [23C25]. And CCR3 and CCR4 are implicated in Th2 cells whereas CXCR3 and CCR5 are associated with Th1 cells [14]. On the flip side, genetic studies further showed that deficiency in CXCR3 and CCR2 accelerated AID in NOD mice [26, 27]. In contrast, CCR5 ablation delayed AID [27], which was contradictory to one publication indicating that CCR5 positively regulated AID [28]. Anti-CXCL10 was reported to delay AID in NOD mice, implying that CXCR3 may accelerate AID [29]. Overexpression of D6 in pancreatic CPHPC islets reduced AID in NOD mice [30]. Overexpression of CCL2, a natural ligand for DARC, D6, and CCR2, in the pancreas reduced AID in NOD mice [31], which is usually consistent with a negative regulation of AID by CCR2, D6, and DACR. Of them, the impact of DARC in AID is usually unclear. 1.3. Mouse Models of AID Animal models are indispensable.The above biochemical cascades lead to cell chemotaxis and other cell functions (Determine 4(a)) [16]. action, and therapeutic potential of the anthraquinones in autoimmune diabetes, including a new strategy for the use of the anthraquinones in autoimmune diabetes. 1. Autoimmune Diabetes 1.1. Etiology and Therapies for Autoimmune Diabetes Autoimmune diabetes (AID) is usually a life-threatening metabolic disease that is initiated and progresses through a complex interplay of environmental, genetic, and immune factors. As a result, insulin-producing subunit to guanosine triphosphate and the dissociation of the Gsubunit from your Gsubunit. This activates protein tyrosine kinases, mitogen-activated protein (MAP) kinases, and phospholipase C. Secondary messengers, inositol triphosphate and diacylglycerol, which are converted from phosphatidylinositol by phospholipase C, induce cellular calcium influx and translocation/activation of proteins kinase C, respectively. The above mentioned biochemical cascades result in cell chemotaxis and additional cell features (Shape 4(a)) [16]. Therefore, chemokines/chemokine receptors have already been proposed as medication focuses on for inflammatory illnesses [14, 17C19]. For example, the 1st FDA authorized CXCR4 antagonist, plerixafor/AMD3100, can be used to mobilize hematopoietic stem cells, that are gathered for make use of in stem cell graft in individuals with hematological malignancies. Plerixafor was developed to hinder SDF-1/CXCR4 discussion and shows guarantee for HIV disease, malignancies, and autoimmune illnesses such as arthritis rheumatoid [20]. Nevertheless, this drug can be expensive due to the issue in its total synthesis. There is certainly, consequently, a demand for CPHPC the finding of fresh CXCR4 antagonists that are both cost-effective and powerful. Open in another window Shape 2 Chemokines and their cognate receptors. Twenty-three chemokine receptors and their organic ligands are categorized into CCR, CXCR, and additional categories. Open up in another window Shape 4 Setting of actions of catenarin and additional anthraquinones for Help. (a) Upon chemokine binding, a chemokine receptor can be triggered and induces G proteins activation. A cascade of calcium mineral mobilization and activation/phosphorylation of MAPKK/MAPK pathways qualified prospects to chemotaxis of leukocytes and, consequently, insulitis and diabetes. (b) Catenarin and CPHPC most likely additional anthraquinones inhibit leukocyte migration mediated by CCR5 and CXCR4 via the inactivation of MAPKs (p38 and JNK), MKKs (MKK6 and MKK7), and calcium mineral mobilization. Because of this, anthraquinones can suppress insulitis and diabetes. Since T cells and additional leukocytes are usually important players in Help [3, 21], disturbance with chemokine receptors in leukocytes is actually a guaranteeing strategy for dealing with insulitis and Help prophylaxis. CXCR4 can be expressed in every the leukocytes including na?ve T cells [22]. CCR5 can be preferentially indicated in triggered T cells and macrophages [23C25]. And CCR3 and CCR4 are implicated in Th2 cells whereas CXCR3 and CCR5 are connected with Th1 cells [14]. On the other hand, genetic research further demonstrated that insufficiency in CXCR3 and CCR2 accelerated Assist in NOD mice [26, 27]. On the other hand, CCR5 ablation postponed Help [27], that was contradictory to 1 publication indicating that CCR5 favorably regulated Help [28]. Anti-CXCL10 was reported to hold off Assist in NOD mice, implying that CXCR3 may accelerate Help [29]. Overexpression of D6 in pancreatic islets decreased Assist in NOD mice [30]. Overexpression of CCL2, an all natural ligand for DARC, D6, and CCR2, in the pancreas decreased Assist in NOD mice [31], which can be consistent with a poor regulation of Help by CCR2, D6, and DACR. Of these, the effect of DARC in Help can be unclear. 1.3. Mouse Types of Help Animal versions are essential for dissecting pathogenesis as well as for preclinical tests in Help despite some difference between pet models and.Occurring Anthraquinones Naturally 2.1. Etiology and Therapies for Autoimmune Diabetes Autoimmune diabetes (Help) can be a life-threatening metabolic disease that’s initiated and advances through a complicated interplay of environmental, hereditary, and immune elements. Because of this, insulin-producing subunit to guanosine triphosphate as well as the dissociation from the Gsubunit through the Gsubunit. This activates proteins tyrosine kinases, mitogen-activated proteins (MAP) kinases, and phospholipase C. Supplementary messengers, inositol triphosphate and diacylglycerol, that are transformed from phosphatidylinositol by phospholipase C, induce mobile calcium mineral influx and translocation/activation of proteins kinase C, respectively. The above mentioned biochemical cascades result in cell chemotaxis and additional cell features (Shape 4(a)) [16]. Therefore, chemokines/chemokine receptors have already been proposed as medication focuses on for inflammatory illnesses [14, 17C19]. For example, the 1st FDA authorized CXCR4 antagonist, plerixafor/AMD3100, can be used to mobilize hematopoietic stem cells, that are gathered for make use of in stem cell graft in individuals with hematological malignancies. Plerixafor was developed to hinder SDF-1/CXCR4 discussion and shows guarantee for HIV disease, malignancies, and autoimmune illnesses such as rheumatoid arthritis [20]. However, this drug is definitely expensive because of the difficulty in its total synthesis. There is, consequently, a demand for the finding of fresh CXCR4 antagonists that are both cost-effective and potent. Open in a separate window Number 2 Chemokines and their cognate receptors. Twenty-three chemokine receptors and their natural ligands are classified into CCR, CXCR, and additional categories. Open in a separate window Number 4 Mode of action of catenarin and additional anthraquinones for AID. (a) Upon chemokine binding, a chemokine receptor is definitely triggered and induces G protein activation. A cascade of calcium mobilization and activation/phosphorylation of MAPKK/MAPK pathways prospects to chemotaxis of leukocytes and, consequently, insulitis and diabetes. (b) Catenarin and probably additional anthraquinones inhibit leukocyte migration mediated by CCR5 and CXCR4 via the inactivation of MAPKs (p38 and JNK), MKKs (MKK6 and MKK7), and calcium mobilization. As a result, anthraquinones can suppress insulitis and diabetes. Since T cells and additional leukocytes are thought to be essential players in AID [3, 21], interference with chemokine receptors in leukocytes could be a encouraging approach for treating insulitis and AID prophylaxis. CXCR4 is definitely expressed in all the leukocytes including na?ve T CPHPC cells [22]. CCR5 is definitely preferentially indicated in triggered T cells and macrophages [23C25]. And CCR3 and CCR4 are implicated in Th2 cells whereas CXCR3 and CCR5 are associated with Th1 cells [14]. On the flip side, genetic studies further showed that deficiency in CXCR3 and CCR2 accelerated AID in NOD mice [26, 27]. In contrast, CCR5 ablation delayed AID [27], which was contradictory to one publication indicating that CCR5 positively regulated AID [28]. Anti-CXCL10 was reported to delay AID in NOD mice, implying that CXCR3 may accelerate AID [29]. Overexpression of D6 in pancreatic islets reduced AID in NOD mice [30]. Overexpression of CCL2, a natural ligand for DARC, D6, and CCR2, in the pancreas reduced AID in NOD mice [31], which is definitely consistent with a negative regulation of AID by CCR2, D6, and DACR. Of them, the effect of DARC in AID is definitely unclear. 1.3. Mouse Models of AID Animal models are indispensable for dissecting pathogenesis and for preclinical tests in AID despite some difference between animal models and individuals. The animal models include streptozotocin- (STZ-) treated mice, nonobese diabetic (NOD) mice, Biobreeding (BB) rats, Very long Evans Tokushima Slim (LETL) rats, New Zealand white rabbits, Chinese hamsters, Keeshond dogs, and Celebes black apes [12]. 2. Naturally Occurring Anthraquinones 2.1. Chemical.quantity /th th align=”center” rowspan=”1″ colspan=”1″ Name /th th align=”center” rowspan=”1″ colspan=”1″ Classification /th th align=”center” rowspan=”1″ colspan=”1″ Molecular method /th th align=”center” rowspan=”1″ colspan=”1″ Biological activities /th /thead 72CatenarinAnthraquinoneC15H10O6 Antichemotactic [28] and antidiabetic [28]69Emodin AnthraquinoneC15H10O5 Antichemotactic [67] and antidiabetic [67]44PhyscionAnthraquinoneC16H12O5 Antichemotactic [28] 70Cascarin AnthraquinoneC21H20O9 Antichemotactic [28]71Rhein AnthraquinoneC15H8O6 Antichemotactic [28]77DiacereinAnthraquinoneC19H12O8 Antiosteoarthritic [68] and antidiabetic [28] Open in a separate window Diacerein is a commercial drug commonly utilized to treat human being osteoarthritis. immune rules. We discuss the structure and activity relationship, mode of action, and restorative potential of the anthraquinones in autoimmune diabetes, including a new strategy for the use of the anthraquinones in autoimmune diabetes. 1. Autoimmune Diabetes 1.1. Etiology and Therapies for Autoimmune Diabetes Autoimmune diabetes (AID) is definitely a life-threatening metabolic disease that is initiated and progresses through a complex interplay of environmental, genetic, and immune factors. As a result, insulin-producing subunit to guanosine triphosphate and the dissociation of the Gsubunit from your Gsubunit. This activates protein tyrosine kinases, mitogen-activated protein (MAP) kinases, and phospholipase C. Secondary messengers, inositol triphosphate and diacylglycerol, which are converted from phosphatidylinositol by phospholipase C, induce cellular calcium influx and translocation/activation of protein kinase C, respectively. The above biochemical cascades lead to cell chemotaxis and additional cell functions (Number 4(a)) [16]. Hence, chemokines/chemokine receptors have been proposed as drug focuses on for inflammatory diseases [14, 17C19]. For instance, the 1st FDA authorized CXCR4 antagonist, plerixafor/AMD3100, is used to mobilize hematopoietic stem cells, which are collected for use in stem cell graft in individuals with hematological cancers. Plerixafor was initially developed to interfere with SDF-1/CXCR4 connection and shows promise for HIV illness, cancers, and autoimmune diseases such as rheumatoid arthritis [20]. However, this drug is definitely expensive because of the difficulty in its total synthesis. There is, consequently, a demand for the finding of fresh CXCR4 antagonists that are both cost-effective and potent. Open in a separate window Number 2 Chemokines and their cognate receptors. Twenty-three chemokine receptors and their natural ligands are classified into CCR, CXCR, and additional categories. Open in a separate window Number 4 Mode of action of catenarin and additional anthraquinones for AID. (a) Upon chemokine binding, a chemokine receptor is definitely triggered and induces G proteins activation. A cascade of calcium mineral mobilization and activation/phosphorylation of MAPKK/MAPK pathways network marketing leads to chemotaxis of leukocytes and, eventually, insulitis and diabetes. (b) Catenarin and most likely various other anthraquinones inhibit leukocyte migration mediated by CCR5 and CXCR4 via the inactivation of MAPKs (p38 and JNK), MKKs (MKK6 and MKK7), and calcium mineral mobilization. Because of this, anthraquinones can suppress insulitis and diabetes. Since T cells and various other leukocytes are usually important players in Help [3, 21], disturbance with chemokine receptors in leukocytes is actually a appealing approach for dealing with insulitis and Help prophylaxis. CXCR4 is normally expressed in every the leukocytes including na?ve T cells [22]. CCR5 is normally preferentially portrayed in turned on T cells and macrophages [23C25]. And CCR3 and CCR4 are implicated in Th2 cells whereas CXCR3 and CCR5 are connected with Th1 cells [14]. On the other hand, genetic research further demonstrated that insufficiency in CXCR3 and CCR2 accelerated Assist in NOD mice [26, 27]. On the other hand, CCR5 ablation postponed Help [27], that was contradictory to 1 publication indicating that CCR5 favorably regulated Help [28]. Anti-CXCL10 was reported to hold off Assist in NOD mice, implying that CXCR3 may accelerate Help [29]. Overexpression of D6 in pancreatic islets decreased Assist in NOD mice [30]. Overexpression of CCL2, an all natural ligand for DARC, D6, and CCR2, in the pancreas decreased Assist in NOD mice [31], which is normally consistent with a poor regulation of Help by CCR2, D6, and DACR. Of these, the influence of DARC in Help is normally unclear. 1.3. Mouse Versions.
They could be formed either with the cyclization of linear octa-[40], [41],[32],and[42]22-(Hydroxymethyl)-AQH HOCH2 HHHHHH [43] and??[44]32-Methoxy-AQH MeO HHHHHH [42]42-Hydroxy-AQH OH HHHHHH [42]51-Methoxy-AQOH H HHHHHH [45, 46]61-Hydroxy-2-methyl AQOH Me personally HHHHHH [42][46][39][39][39], [39], andRubia yunnanensis[43]71-Hydroxy-2-(hydroxymethyl)-AQOH HOCH2 HHHHHH [32]82-(Ethoxycarbonyl)-1-hydroxy-AQOH EtOOC HHHHHH [39]91-Methoxy-2-methyl-AQMeO Me personally HHHHHH [39],[39], and[47]11Alizarin 2-methyl ether[42][39],[32], and [47]12Alizarin 1-methyl ether[42]13Alizarin 1,2-dimethyldiether[42]14Rubiadin (1,3-dihydroxy-2-[40][42][32], and[39],Rubia yunnanensis[43]15Lucidin (1,3-dihydroxy-2-[32][42], and[33]16Nordamnacanthal (1,3-dihydroxy-2-formyl-AQ)OHCHOOHHHHHH [32] and Rubia iberica[33] 17Munjistin (1,3-dihydroxy-2-carboxy-AQ)OHHOOCOHHHHHH [42]181,3-Dihydroxy-2-(methoxycarbonyl)-AQOHMeOOCOHHHHHH [32]192-(Ethoxymethyl)-1,3-dihydroxy-AQOHEtOCH2 OHHHHHH [32]201,3-Dihydroxy-2-(methoxymethyl)-AQOHMeOCH2 OHHHHHH [32] 21Lucidin dimethyl etherMeOHHOCH2 MeOHHHHH [39]22Munjistin dimethyl ether (2-carboxy-[32]232-BenzylxanthopurpurinOHPhCH2 OHHHHHH [32]24Anthragallol 3-methyl etherOHOHMeOHHHHH [42]25Anthragallol 2,3-dimethyl etherOHMeOMeOHHHHH [32] 262-Carboxy-1-hydroxy-3-methoxy-AQOHHOOCMeOHHHHH [48]273-Hydroxy-1-methoxy-2-(methoxymethyl)-AQMeOMeOCH2 OHHHHHH [49]28Anthragallol (1,2,3-trihydroxy-AQ)OHOHOHHHHHH [32]29Purpurin (1,2,4-trihydroxy AQ)OHOHHOHHHHH [32, 42][32][33][33], andRubia tetragona[32]30Quinizarin (1,4-dihydroxy-AQ)OHHHOHHHHH [32] andRubia tinctorum[32]311,4-Dihydroxy-2-(hydroxymethyl)-AQOHHOCH2 HOHHHHH [32] andRubia yunnanensis[32]322-(Ethoxycarbonyl)-1,4-dihydroxy-AQOHEtOOCHOHHHHH [32]33Christophine (2-(ethoxymethyl)-[32]341,4-Dihydroxy-2-methyl-AQOHMeHOHHHHH [32] and [32]35Xanthopurpurin (1,3-dihydroxy-AQ)OHHOHHHHHH [32][32][39][43],36Xanthopurpurin 3-methyl ether[32]37Xanthopurpurin dimethyl ether (1,3-dimethoxy-AQ)MeOHMeOHHHHH [32] 381-Hydroxy-3-(methoxycarbonyl)-AQOHHMeOOCHHHHH [32], [39], and [39]39Pseudopurpurin (3-(carboxy)-1,2,4-trihydroxy-AQ)OHOHHOOCOHHHHH [32][32][32]401,4-Dihydroxy-2-methyl-5-methoxy-AQOHMeHOHMeOHHH [50]411,4-Dihydroxy-2-methyl-8-methoxy-AQOHMeHOHHHHMeO [50]421,4-Dihydroxy-6-methyl-AQOHHHOHHMeHH [51]431,5-Dihydroxy-2-methyl-AQOHMeHHOHHHH [51]44Physcion (1,8-dihydroxy-3-methoxy-6-methyl-AQ)OHHMeHHMeHOH [50] and[52]452-Methyl-1,3,6-trihydroxy-AQOHMeOHHHOHHH [32][32][43], [32], and[32]461,4-Dihydroxy-7-methyl-AQOHHHOHHHMeH [50]474,5-Dihydroxy-2-methoxy-7-methyl-AQHMeHOHOHHMeOH [50]482,7-Dihydroxy-4-methoxy-3-methyl-AQHOHMeMeOHHOHH [32]492-Hydroxy-7-methyl-AQHMeHHHHOHH [32]502-Carboxy-4-hydroxy-AQHHOOCHOHHHHH [32] 51 3-([32]523-(6-O-Acetyl-[32] 533-[(2-O-6-Deoxy-[32], [32][39],[43] 543-[(3-O-Acetyl-2-O-6-deoxy-[32]553-[(6-O-Acetyl-2-O-6-deoxy-[32][39],[43][32]563-[(3,6-O-Diacetyl-2-O-6-deoxy-[32]573-[(4,6-O-Diacetyl-2-O-6-deoxy-[32]583-[(4-O-Acetyl-2-O-6-deoxy-[32]593-[(6-O-Acetyl-2-O-[32]60Ruberythric acidity (1-hydroxy-2-[(6-O-[32][32], and?[45]61Lucidin primeveroside (1-hydroxy-2-(hydroxymethyl)-3-[(6-O-[32][32][45], and [32] 632-[(6-O-[32] and[32]643-[(2-O-6-Deoxy-[32]653-([32]663-([32] 672-([32]683-([32]69Emodin (1,3,8-trihydroxy-6-methyl-AQ)OHHMeHHOHHOH [28, 52]70Cascarin (emodin 6-O-rhamnoside)OHHMeHHRhaOHOH [28]73Aloe-emodin (1,8-dihydroxy 3-hydroxy methyl anthraquinone)OHHCH2OHHHHHOH [53], [53], andRheum rhaponticum[53]74Chrysophanol (1,8-dihydroxy-3-methyl-AQ)OHHMeHHMeOHOH Fallopia japonicaF
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