Cardamom And Its Use In Cancer

CARDAMOM

Cardamom shows evidence in a number of trials in various systemic inflammatory conditions. There is reasonable evidence that supplementation in the 3 g daily range sustained over time can reduce key inflammatory markers including IL-6 and c-reactive protein.

Interestingly, together with a low calorie diet, cardamom can also reduce levels of steroidal hormomes dehydroepiandrosterone and androstenedione. Higher levels of these androgens are known to increase progression rates of hormone driven cancers such as breast and prostate.

TYPICAL ABSORPTION LEVELS

20 – 30%

EXAMPLES OF IMPROVED OUTCOMES

PRE-DIAGNOSIS OR PREVENTION

Highlighted Studies

…cardamom significantly reduced the levels of inflammatory factors, including hs‐CRP (SMD: −0.60 mg/dL, IL‐6 (WMD: −1.25 mg/dL; TNF‐α (WMD: −2.10 ), and measures of systolic (WMD: −0.54 mmHg, p = .002) and diastolic (WMD: −0.90 mmHg;) blood pressure. The current meta‐analysis showed that cardamom can help reduce inflammation and improve blood pressure.

Among androgen hormones, luteinizing hormone, androstenedione, and dehydroepiandrosterone were significantly decreased , and follicle-stimulating hormone was significantly increased in the green cardamom group. Our findings showed that TNF-α, IL-6, and CRP serum levels were significantly decreased after the intervention with green cardamom plus low-calorie diet. In addition, the expression levels of TNF-α and CRP genes were significantly decreased in the intervention group

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This trial for the first time assessed the effects of GC on blood inflammatory biomarkers, liver enzymes, and Sirt1 in [non alcoholic fatty liver disease ] patients. According to time-by-treatment interaction effect.., ALT, IL-6, TNF-α, and hs-CRP decreased and Sirt1 increased significantly among cardamom group … Moreover, the improvements in the degree of fatty liver in cardamom group was significantly higher than the placebo group.

Cardamom could improve some parameters of inflammation and oxidative stress in pre-diabetic subjects. Thus it may be useful in reducing complications associated with inflammation and oxidative stress…cardamom supplementation significantly decreased serum hs-CRP and hs-CRP:IL-6 ratio [inflammatory markers implicated in cancer progression]

TABLE OF REFERENCES

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https://pmc.ncbi.nlm.nih.gov/articles/PMC10804083/	2	The results showed that cardamom significantly reduced the levels of inflammatory factors, including hs‐CRP (SMD: −0.60 mg/dL), IL‐6 (WMD: −1.25 mg/dL), TNF‐α (WMD: −2.10 kg), and measures of systolic (WMD: −0.54 mmHg) and diastolic (WMD: −0.90 mmHg) blood pressure. The current meta‐analysis showed that cardamom can help reduce inflammation and improve blood pressur	although hs‐CRP did not change significantly in studies that lasted less than 10 weeks, a significant reduction was observed in studies conducted for greater or equal to 10 weeks. Moreover, subgroup analysis based on sex (male vs. female) showed a significant reduction in the level of hs‐CRP. In line with the current results, a clinical trial reported that 3 g of cardamom combined with a low‐calorie diet over 16 weeks reduced serum levels of inflammatory factors including TNF‐α, IL‐6, and hs‐CRP
https://scijournals.onlinelibrary.wiley.com/doi/10.1002/jsfa.8414	2	Cardamom could improve some parameters of inflammation and oxidative stress in pre-diabetic subjects. Thus it may be useful in reducing complications associated with inflammation and oxidative stress in these patients.	After the adjustment of some covariates, cardamom supplementation significantly decreased serum hs-CRP (P = 0.02), hs-CRP:IL-6 ratio (P = 0.008), and MDA (P = 0.009) compared with the placebo group.
https://link.springer.com/article/10.1007/s40519-021-01223-3	2	This study showed that green cardamom plus low-calorie diet significantly reduces TNF-α, IL-6, and CRP serum (P < 0.001) (Table 3 and Fig. 3a, c, e). In addition, we observed that the expression level of TNF-α and CRP genes was significantly decreased after the intervention with green cardamom plus low-calorie diet	Green cardamom is an excellent source of essential oils, flavonoids, polyphenols, and sterols with analgesic, anti-inflammatory, antimicrobial and antioxidant properties [29]. The findings of our study showed the effect of the green cardamom on reducing inflammation by down-regulated the expression of inflammatory genes.
https://pmc.ncbi.nlm.nih.gov/articles/PMC6156864/	1.5	GC supplementation in obese NAFLD patients reduced inflammatory biomarkers (IL-6, TNF-α, and hs-CRP), ALT, and the degree of fatty liver and increased Sirt1 compared with placebo. Accordingly, GC may be useful in other metabolic diseases associated with inflammation.	According to time-by-treatment interaction effect in both unadjusted and adjusted analysis model, ALT, IL-6, TNF-α, and hs-CRP decreased and Sirt1 increased significantly among cardamom group in comparison with the placebo group. Moreover, the improvements in the degree of fatty liver in cardamom group was significantly higher than the placebo group
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5623966/	1.5	However, TC and LDL-C significantly decreased and insulin sensitivity increased in the cardamom group. Furthermore, in the cardamom group, mean HDL-C levels were maintained while in the control group, there was a significant decrease after the study, suggestive of a protective effect of cardamom on HDL-C level. It might be possible that cardamom proves beneficial for subjects with more blood parameters disturbances. Moreover, different results may be obtained by a higher dose of supplement and a longer duration of intervention.	The positive properties of cardamom are mainly due to its volatile oil, which has terpene, esters, flavonoids, and other compounds. The major compounds of the oil are 1, 8 cineole (36.3%) and α-terpinyl acetate (31.3%) [21]. 1, 8 -cineole, a monoterpenic oxide, has vascular relaxant, anti-inflammatory, and antioxidant properties [22–24]. In addition, studies show that the health effects of spices are related to their flavonoids component, so similar effects of different spices on blood pressure, glucose indices, and lipid profile can largely be explained by their flavonoids content as well.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808032/	1	In conclusion, cardamonin suppresses existing breast CSCs after chemotherapeutic drug treatments, prevents the enrichment of new CSCs during chemotherapeutic drug treatments, and enhances the efficacy of chemotherapeutic drugs by reducing tumor burden as well as the CSC pool in vivo. Cardamonin, which is found in many plant species [15], seems to be a promising candidate in CSC-targeted therapies either concurrently used with chemotherapeutic drugs or after chemotherapeutic treatment.	To determine whether cardamonin with doxorubicin reduces the CSC pool in vivo, we harvested tumors after three cycles of treatment and assessed the CD44high/CD24−/low subpopulation using flow cytometry. Notably, the CSC population in tumors harvested from mice receiving doxorubicin alone increased 2.5-fold over those receiving vehicle alone, although the tumor weights were lower and sizes smaller (Figure (Figure5C).5C). In contrast, co-administration of cardamonin and doxorubicin not only remarkably reduced the tumor growth but also abolished doxorubicin-enriched CSCs in mouse xenografts
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0127778	1	In summary, these results demonstrated that cardamonin inhibited the progression of cancer cells by several mechanisms including inhibition of proliferation, repression of migration and metastasis. Our data showed that cardamonin inhibited the metastatic potential of LLC cells in vitro/vivo through regulating the mTOR mediated expression of E-cadherin. It suggested that cardamonin might be of value in developing as an anti-cancer agent.	Dramatically, no marked hepatotoxicity and nephrotoxicity were found in rats treated with cardamonin, suggesting that cardamonin had a better safety in vivo than rapamycin [15]. Because rapamycin exerts various adverse reactions during its application, cardamonin might have more clinical values as a potential mTOR inhibitor. Furthermore, cardamonin has nephroprotective effect against cisplatin induced renal injury through suppressing oxidative stress and inflammation in rats [30]. It prompts us to investigate its antitumor effect when combination with cisplatin
https://jeccr.biomedcentral.com/articles/10.1186/s13046-019-1351-4#	1	Our results reveal novel function of cardamonin in inhibiting the HIF-1α pathway and its dependent metabolic reprogramming in breast cancer cells (Fig. 8). We also identified the mTOR/p70S6K pathway as one of the cardamonin targets to repress HIF-1α/PDHK1 axis. These findings provide the mechanistic insight into tumor inhibitory activity of cardamonin and suggest the therapeutic potential of cardamonin in breast cancer treatment.	We also found that cardamonin inhibited the Nrf2-dependent ROS scavenging system which further increased intracellular ROS levels. Eventually, accumulation of the intracellular ROS induced apoptosis in breast cancer cells. In addition, cardamonin treatment reduced glucose uptake as well as lactic acid production and efflux, suggesting its function in repressing the glycolysis process.
https://www.oncotarget.com/article/5819/text/	1	In this report, we provide the first demonstration that cardamonin, a small molecule, selectively inhibits breast CSCs that have been enriched by chemotherapeutic drugs. In addition, cardamonin also sufficiently prevents the enrichment of CSCs when simultaneously used with chemotherapeutic drugs. Specifically, cardamonin effectively abolishes chemotherapeutic drug-induced up-regulation of IL-6, IL-8 and MCP-1 and activation of NF-κB/IKBα and Stat3. Furthermore, in a xenograft mouse model, co-administration of cardamonin and the chemotherapeutic drug doxorubicin significantly retards tumor growth and simultaneously decreases CSC pools in vivo. Since cardamonin has been found in some herbs, this work suggests a potential new approach for the effective treatment of breast CSCs by administration of cardamonin either concurrent with or after chemotherapeutic drugs.	MCP-1 has been found to enhance stem cell phenotypes and CSC self-renewal in breast cancer [46], and facilitate the generation of induced pluripotent stem cells [52]. It is also well known that NF-κB and Stat3 pathways govern cytokine productions in response to different stimuli, are associated with drug resistance, and regulate tumor angiogenesis and invasiveness [16, 44, 45, 50, 53–55]. Significantly, our results show that cardamonin is capable of effectively repressing IL-6, IL-8 and MCP-1 up-regulation and NF-κB and Stat3 activation, suggesting a possible mechanism underlying cardamonin inhibitory effects on CSC enrichment induced by chemotherapeutic drugs.
https://www.sciencedirect.com/science/article/pii/S0753332220313482	1	We found that P38 inhibitor and JNK inhibitor neutralized the CAR-induced inhibitory effect to some degree, leading to a partially restored ability of proliferation, migration and invasion in OS cells. In conclusion, our study validate that CAR can inhibit the growth of OS [Osteosarcoma] in vitro and in vivo possibly through activating P38 and JNK signaling pathways. Notably, we confirm that CAR has relative lower toxicity against normal cells. Our findings may suggest the clinical potential of CAR to become an efficacious drug candidate for the OS treatment.	Among these MMPs, MMP-2 is proved to essential for tumor metastasis and invasion because it can remodel the basement membrane by degrading type IV collagen [39,40]. In this study, we found that CAR treatment inhibited cell migration and invasion, and reduced the MMP-2 protein level of OS cells. Collectively, our results suggest that CAR may inhibit migration and invasion of OS cells possibly through reversing EMT process and inhibiting MMP-2.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440626/	1	Treated with cardamonin, the proliferation, invasion and migration of LLC cells were significantly inhibited. The expression of Snail was decreased by cardamonin, while that of E-cadherin was increased. In addition, cardamonin inhibited the activation of mTOR and its downstream target ribosomal S6 kinase 1 (S6K1). Furthermore, the tumor growth and its lung metastasis were inhibited by cardamonin in C57BL/6 mice. It indicated that cardamonin inhibited the invasion and metastasis of LLC cells through inhibiting mTOR. The metastasis inhibitory effect of cardamonin was correlated with down-regulation of Snail and up-regulation of E-cadherin.	hese results demonstrated that cardamonin inhibited the progression of cancer cells by several mechanisms including inhibition of proliferation, repression of migration and metastasis. Our data showed that cardamonin inhibited the metastatic potential of LLC cells in vitro/vivo through regulating the mTOR mediated expression of E-cadherin. It suggested that cardamonin might be of value in developing as an anti-cancer agent.
https://www.researchgate.net/publication/330499027_Cardamonin_inhibits_the_proliferation_and_metastasis_of_non-small-cell_lung_cancer_cells_by_suppressing_the_PI3KAktmTOR_pathway	1	The explorations of the underlying mechanisms suggested that cardamonin exer- ted anticancer effects through the suppression of the PI3K/ Akt/mTOR pathway. Collectively, our data indicate that cardamonin might be a rational natural ingredient for NSCLC treatment and suggest that pharmacological agents that target the PI3K/Akt/mTOR pathway might be promising therapeutic strategies for cancers	Further study showed that cardamonin reduced the phosphorylation levels of the downstream effectors of phosphoinositide 3-kinase (PI3K), including protein kinase-B (Akt/PKB) and mammalian target of rapamycin (mTOR). Moreover, in the H460 xenograft model, cardamonin significantly retarded tumor growth. Also, in tumor tissues, we found that cardamonin treatment decreased the expression rates of Ki-67, p-Akt, and p-mTOR. These data suggest that cardamonin suppressed NSCLC cell proliferation and inhibited metastasis partly by restraining the PI3K/Akt/mTOR pathway and it might be an effective therapeutic compound for NSCLC in the future.