EMODIN

Also known as chinese rhubarb.  Pre-clinical testing indicate support of metabolic health via glucose and lipid control but no evidence from human clinical trials. Only one older trial showing reductions radiation induced lung toxicity from radiotherapy , where lower inflammatory markers were also reported (see References)

Lab studies show actions on many cancers and metastasis, including liver, colon, pancreas, ovarian cancers, but again no clincial trials to validate these pre-clinical actions

TYPICAL ABSORPTION LEVELS

20 – 50%

EXAMPLES OF IMPROVED OUTCOMES

NO

PRE-DIAGNOSIS OR PREVENTION

Highlighted Studies

Emodin reduced lipid synthesis [lab model] by inhibiting the expression of triglyceride (TG) synthesis-related genes, such as fatty acid synthase (Fasn),and ultimately reduced liver metastasis in breast cancer [Lab study].. emodin may have therapeutic potential in the prevention or treatment of breast cancer liver metastasis.

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Pulmonary metastasis of the ovarian cancer cells was significantly suppressed in the tumor mouse model by the administration of emodin….emodin significantly reduced the proportion of ovarian cancer stem-like cells in metastatic lung tissues. In conclusion, emodin, a potent inhibitor of EMT, could serve as a potential candidate for ovarian cancer therapy.

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..emodin inhibited migration and invasion of MDA-MB-231 cells [Lab study], and also inhibited the expression levels of p-p38 and p-ERK1/2, MMP-2, MMP-9 and uPA. Collectively, the present study suggests that emodin is a non-specific protein kinase inhibitor affecting p38, ERK and proteolytic enzymes, MMPs and uPA in inhibiting invasion of breast cells.

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..our study provides direct evidence for the attenuation by emodin of the high metastatic potential to the liver in the state of obesity and hyperlipidemia induced by a HFD through the AKT and ERK signaling pathways interacting with CK2α in breast cancer
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TABLE OF REFERENCES

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https://pubmed.ncbi.nlm.nih.gov/17870203/1.5 The rhubarb extract significantly attenuated RILT and improved PF, probably by decreasing the level of TGF-beta1 and IL-6. These results may be of value for the prophylaxis of Radiation induced lung toxicity RILT, but the exact mechanisms underlying these prophylactic effects remain to be further explored.he incidence of RILT in the trial group was significantly lower than that in the control group at 6 weeks and 6 months after treatment (32.4% versus 56.7% at week 6, and 27.0% versus 52.8% at month 6, both P<0.05). The plasma TGF-beta1 levels in the trial group were significantly lower than that in the control group during and after the treatment (P<0.05 or 0.01, respectively). The serum IL-6 levels in the trial group were significantly lower than that in the control group during the treatment
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10361095/#1These results demonstrate the potential of CK2α as a clinical target in breast cancer. Additionally, emodin also decreased the proliferation and invasiveness of breast cancer cells. These studies were consistent with previous work indicating that emodin attenuates breast cancer cell metastasis and angiogenesis via MMPs, VEGFR, and EMT inhibition [22,23]. The inhibition of breast cancer cells through the AKT and ERK pathways via interaction with CK2α may be another one of the mechanisms by which emodin inhibits liver metastasis in breast cancer.Emodin reduced lipid synthesis by inhibiting the expression of triglyceride (TG) synthesis-related genes, such as fatty acid synthase (Fasn), glycerol-3-phosphate acyltransferase 1 (Gpat1), and stearoyl-CoA desaturase (Scd1), and ultimately reduced liver metastasis in breast cancer. In addition, emodin inhibited breast cancer cell proliferation and invasion through the serine/threonine kinase (AKT) signaling and extracellular-regulated protein kinase (ERK) pathways by interacting with CSNK2A1, ESR1, ESR2, PIM1 and PTP4A3. Our results indicate that emodin may have therapeutic potential in the prevention or treatment of breast cancer liver metastasis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8822392/1Thus, elimination of CSCs in the tumor microenvironment could be a promising strategy to conquer ovarian cancer metastasis. In the present study, it was demonstrated that emodin could reduce the proportion of ovarian CSC in metastatic lung tissues, suggesting that emodin suppressed pulmonary metastasis of ovarian cancer. In summary, the present study provided important information regarding the antitumor activities of emodin in ovarian cancer. Emodin exhibited antitumor and anti-metastasis effects on ovarian cancer by inhibiting EMT and ovarian CSC formation....emodin could serve as a potential drug for treating ovarian cancer and metastasis.As emodin reduced the migratory and invasion ability of the ovarian cancer cell lines, the anti-metastasis effect of emodin was investigated using a pulmonary metastasis tumor mouse model. The results showed that administration of emodin, at 20 and 40 mg/kg, significantly inhibited lung metastasis of ovarian cancer, which was consistent with the in vitro experiments. Furthermore, poor outcomes of ovarian cancer therapies are usually caused by a small proportion of CSCs, that have escaped from the primary cancer lesion (60). Thus, elimination of CSCs in the tumor microenvironment could be a promising strategy to conquer ovarian cancer metastasis.Screenshot from 2024-02-12 15-46-03
https://www.spandidos-publications.com/10.3892/or.2014.35851emodin inhibited lung metastasis in mice bearing the breast cancer MDA-MB-231 xenografts with no obvious changes in body weight, liver and kidney functions. These results indicated that emodin inhibited the lung metastasis of human breast cancer in a mouse xenograft model, and inhibited the invasion of MDA-MB-231 cells associated with the downregulation of MMP-2, MMP-9, uPA and uPAR expression as well as decreased activity of p38 and ERK.There is previous evidence that emodin inactivated ERK1/2 in lung cancer H1703 or A549 cells and reduced the phosphorylation of the p38 MAPK in atherosclerosis (46). In breast cancer, emodin suppressed HER-2/neu tyrosine kinase activity in MDA-MB-435 cells, which overexpressed HER-2/neu and thereby suppressing the proliferation of these cells (47). In the present study, we found that emodin inhibited migration and invasion of MDA-MB-231 cells, and also inhibited the expression levels of p-p38 and p-ERK1/2, MMP-2, MMP-9 and uPA. Collectively, the present study suggests that emodin is a non-specific protein kinase inhibitor affecting p38, ERK and proteolytic enzymes, MMPs and uPA in inhibiting invasion of breast cellsScreenshot from 2024-02-12 15-49-22
https://www.spandidos-publications.com/10.3892/mmr.2018.93041The data of our research suggested that miR-1271 significantly decreased in pancreatic cancer cells and tissues. Twist1 may be a target gene of miR-1271. MiR-1271 significantly inhibited pancreatic cancer cell SW1990 EMT and invasive ability, and emodin could inhibit SW1990 cell EMT by raising the level of miR-1271. In addition, we found that emodin inhibited the liver metastasis of pancreatic cancer by inhibiting EMT in vivo. We provide theoretical and experimental evidence for the further development of miRNA-based targeted therapy of pancreatic cancer.Emodin administration significantly increased the level of miR-1271 and mRNA level of E-cadherin in pancreatic cancer hepatic metastasis tissues (Fig. 7B). The results of western blot analysis (Fig. 7A) and immunohistochemistry (Fig. 7C) showed that emodin administration significantly increased E-cadherin protein level, however, the expression of ZEB1 and Twist1 protein significantly decreased. In vivo experiments showed that emodin can inhibit the EMT of pancreatic cancer cells by increasing the content of miR-1271 in pancreatic cancer, and then exert the therapeutic and preventive effects on the metastasis of pancreatic cancer.Screenshot from 2024-02-12 15-54-58
https://pdfs.semanticscholar.org/a7e4/55cfea73e818d986f045c7215be43fb7dcfc.pdf1A Wnt/b-catenin signaling pathway agonist abolished the effect of emodin on EMT and cell mobility, suggesting that emodin exerted its regulating role through the Wnt/b-catenin pathway. The CC xenograft model was established to study the antitumor efficiency of emodin in vivo. The in vivo study further demonstrated that emodin (40 mg/kg) suppressed tumor growth by inhibiting EMT via the Wnt/b-catenin signaling pathway in vivo. Taken together, we suggest that emodin inhibits the invasion and migration of CC cells in vitro and in vivo by blocking EMT, which is related with the inhibition of the Wnt/b-catenin signaling pathwayIn our study, we showed that miR-1271 may act on ZEB1 and TWIST1 at the post-transcriptional phase, but not the mRNA level. In addition, we found that emodin can inhibit the EMT of pancreatic cancer cells by increasing the level of miR-1271 in pancreatic cancer cells. In vivo experiments showed that emodin can inhibit the EMT of pancreatic cancer cells by increasing the content of miR-1271 in pancreatic cancer, and then exert the therapeutic and preventive effects on the metastasis of pancreatic cancer.Screenshot from 2024-02-12 15-58-58

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