Last update
3/18/2026
Reviewed By
Overview
SCIENTIFIC SCORE
Moderately Effective
Based on 7 Researches
8
USERS' SCORE
Good
Based on 2 Reviews
8
Supplement Facts
Serving Size: 1 Vegetable Capsule
Amount Per Serving
%DV
Iron (as iron bisglycinate chelate†)
25 mg
139%
Top Medical Research Studies
9
We explored the effects of rubiadin, a beneficial compound derived from a Chinese herb, on iron metabolism and its implications for liver disease. Recognizing the challenges posed by iron overload diseases, we aimed to discover a safe approach to manage excessive iron accumulation in the body. Through experiments involving various analyses, we observed that rubiadin significantly downregulated proteins that are typically elevated in conditions of high iron, such as transferrin receptor 1 and ferroportin 1.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
Read More
9
We explored how parasitic infection from protoscolex (PSC) impacts liver health, particularly through a process known as ferroptosis, which leads to cell death. In our study, both live rat models and cultured liver cells were used to investigate how PSC infection disrupts iron metabolism, contributing to liver damage.
While we found that ferroptosis resulted from PSC infection, using a ferroptosis inhibitor called Ferrostatin-1 showed promising results in reducing liver cell damage and preventing the formation of fibrotic cysts. This suggests that targeting ferroptosis could be a new avenue for addressing liver issues caused by PSC infection.
While we found that ferroptosis resulted from PSC infection, using a ferroptosis inhibitor called Ferrostatin-1 showed promising results in reducing liver cell damage and preventing the formation of fibrotic cysts. This suggests that targeting ferroptosis could be a new avenue for addressing liver issues caused by PSC infection.
Read More
8
We explored the effects of Shugan Xiaozhi (SGXZ) decoction on metabolic dysfunction-associated steatohepatitis (MASH), a challenging liver disease. By using various advanced methods, we identified how SGXZ works on a mouse model of MASH.
The results showed that SGXZ decoction can significantly improve liver health by regulating specific pathways involved in cell death. Its therapeutic mechanisms appear to involve the p53/SLC7A11/GPX4 pathway, which plays a role in reducing a specific type of cell death linked to iron metabolism, known as ferroptosis.
Overall, SGXZ decoction shows promise as a treatment option for MASH.
The results showed that SGXZ decoction can significantly improve liver health by regulating specific pathways involved in cell death. Its therapeutic mechanisms appear to involve the p53/SLC7A11/GPX4 pathway, which plays a role in reducing a specific type of cell death linked to iron metabolism, known as ferroptosis.
Overall, SGXZ decoction shows promise as a treatment option for MASH.
Read More
Most Useful Reviews
9
Effective iron supplement
Due to my persistently low haemoglobin levels linked to liver disease, I require ongoing iron supplements. After trying various preparations, I find Solgar chelated iron to be one of the few that genuinely alleviates my iron deficiency. An advantage of Solgar's encapsulated form is that it does not cause gastrointestinal discomfort, thus I recommend opting for chelated iron capsules over tablets, as they are gentler on the system even though slightly pricier.
Read More
2
Insufficient dosage
Unfortunately, the dosage is inadequate for my severe iron deficiency related to liver disease, necessitating long-term use. As is well known, iron supplements can be quite damaging to the liver and hard on the intestines.
Read More
Medical Researches
SCIENTIFIC SCORE
Moderately Effective
Based on 7 Researches
8
- All Researches
9
We explored the effects of rubiadin, a beneficial compound derived from a Chinese herb, on iron metabolism and its implications for liver disease. Recognizing the challenges posed by iron overload diseases, we aimed to discover a safe approach to manage excessive iron accumulation in the body. Through experiments involving various analyses, we observed that rubiadin significantly downregulated proteins that are typically elevated in conditions of high iron, such as transferrin receptor 1 and ferroportin 1.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
Read More
9
We explored how parasitic infection from protoscolex (PSC) impacts liver health, particularly through a process known as ferroptosis, which leads to cell death. In our study, both live rat models and cultured liver cells were used to investigate how PSC infection disrupts iron metabolism, contributing to liver damage.
While we found that ferroptosis resulted from PSC infection, using a ferroptosis inhibitor called Ferrostatin-1 showed promising results in reducing liver cell damage and preventing the formation of fibrotic cysts. This suggests that targeting ferroptosis could be a new avenue for addressing liver issues caused by PSC infection.
While we found that ferroptosis resulted from PSC infection, using a ferroptosis inhibitor called Ferrostatin-1 showed promising results in reducing liver cell damage and preventing the formation of fibrotic cysts. This suggests that targeting ferroptosis could be a new avenue for addressing liver issues caused by PSC infection.
Read More
8
We explored the effects of Shugan Xiaozhi (SGXZ) decoction on metabolic dysfunction-associated steatohepatitis (MASH), a challenging liver disease. By using various advanced methods, we identified how SGXZ works on a mouse model of MASH.
The results showed that SGXZ decoction can significantly improve liver health by regulating specific pathways involved in cell death. Its therapeutic mechanisms appear to involve the p53/SLC7A11/GPX4 pathway, which plays a role in reducing a specific type of cell death linked to iron metabolism, known as ferroptosis.
Overall, SGXZ decoction shows promise as a treatment option for MASH.
The results showed that SGXZ decoction can significantly improve liver health by regulating specific pathways involved in cell death. Its therapeutic mechanisms appear to involve the p53/SLC7A11/GPX4 pathway, which plays a role in reducing a specific type of cell death linked to iron metabolism, known as ferroptosis.
Overall, SGXZ decoction shows promise as a treatment option for MASH.
Read More
8
We investigated how the Biejiajian Pill (BJJP) affects liver cancer cells by regulating a process called ferroptosis. In our experiments, we looked at different groups of hepatocellular carcinoma cells treated with various combinations of BJJP and ferroptosis inducers or inhibitors.
We found that BJJP, particularly at higher doses, significantly increased iron levels and reactive oxygen species, while decreasing important antioxidants in the cells. This indicates that BJJP might play a role in managing liver cancer by influencing cell death pathways, particularly through the p62/Keap1/NRF2 signaling pathway.
We found that BJJP, particularly at higher doses, significantly increased iron levels and reactive oxygen species, while decreasing important antioxidants in the cells. This indicates that BJJP might play a role in managing liver cancer by influencing cell death pathways, particularly through the p62/Keap1/NRF2 signaling pathway.
Read More
8
We explored the rare combination of 46, XY disorders of sex development (DSD) and aceruloplasminaemia (ACP) in a young female patient. Recognizing these two conditions together can be challenging, but it's crucial for proper diagnosis and treatment.
After discovering elevated ferritin levels and further tests, we identified a mutation linked to both disorders. Treatment with deferasirox significantly reduced iron overload, which is vital for preventing organ damage linked to these conditions.
Increasing awareness of these coexisting disorders can lead to better outcomes through timely interventions and genetic testing.
After discovering elevated ferritin levels and further tests, we identified a mutation linked to both disorders. Treatment with deferasirox significantly reduced iron overload, which is vital for preventing organ damage linked to these conditions.
Increasing awareness of these coexisting disorders can lead to better outcomes through timely interventions and genetic testing.
Read More
User Reviews
USERS' SCORE
Good
Based on 2 Reviews
8
- All Reviews
- Positive Reviews
- Negative Reviews
9
Effective iron supplement
Due to my persistently low haemoglobin levels linked to liver disease, I require ongoing iron supplements. After trying various preparations, I find Solgar chelated iron to be one of the few that genuinely alleviates my iron deficiency. An advantage of Solgar's encapsulated form is that it does not cause gastrointestinal discomfort, thus I recommend opting for chelated iron capsules over tablets, as they are gentler on the system even though slightly pricier.
Read More
2
Insufficient dosage
Unfortunately, the dosage is inadequate for my severe iron deficiency related to liver disease, necessitating long-term use. As is well known, iron supplements can be quite damaging to the liver and hard on the intestines.
Read More
Frequently Asked Questions
2
Insufficient dosage
Unfortunately, the dosage is inadequate for my severe iron deficiency related to liver disease, necessitating long-term use. As is well known, iron supplements can be quite damaging to the liver and hard on the intestines.
9
Effective iron supplement
Due to my persistently low haemoglobin levels linked to liver disease, I require ongoing iron supplements. After trying various preparations, I find Solgar chelated iron to be one of the few that genuinely alleviates my iron deficiency. An advantage of Solgar's encapsulated form is that it does not cause gastrointestinal discomfort, thus I recommend opting for chelated iron capsules over tablets, as they are gentler on the system even though slightly pricier.
9
We explored the effects of rubiadin, a beneficial compound derived from a Chinese herb, on iron metabolism and its implications for liver disease. Recognizing the challenges posed by iron overload diseases, we aimed to discover a safe approach to manage excessive iron accumulation in the body. Through experiments involving various analyses, we observed that rubiadin significantly downregulated proteins that are typically elevated in conditions of high iron, such as transferrin receptor 1 and ferroportin 1.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
8
We explored the effects of Shugan Xiaozhi (SGXZ) decoction on metabolic dysfunction-associated steatohepatitis (MASH), a challenging liver disease. By using various advanced methods, we identified how SGXZ works on a mouse model of MASH.
The results showed that SGXZ decoction can significantly improve liver health by regulating specific pathways involved in cell death. Its therapeutic mechanisms appear to involve the p53/SLC7A11/GPX4 pathway, which plays a role in reducing a specific type of cell death linked to iron metabolism, known as ferroptosis.
Overall, SGXZ decoction shows promise as a treatment option for MASH.
The results showed that SGXZ decoction can significantly improve liver health by regulating specific pathways involved in cell death. Its therapeutic mechanisms appear to involve the p53/SLC7A11/GPX4 pathway, which plays a role in reducing a specific type of cell death linked to iron metabolism, known as ferroptosis.
Overall, SGXZ decoction shows promise as a treatment option for MASH.
References
- Minder AE, Granata F, van Breemen F, Schneider-Yin X, Minder EI, et al. Long-term iron supplementation in four patients with X-linked erythropoietic protoporphyria: associations with serum proteins and erythrocyte protoporphyrin levels-a single-centre retrospective study. Front Mol Biosci. 2025;12:1509803. 10.3389/fmolb.2025.1509803
- Xie X, Chang L, Zhu X, Gong F, Che L, et al. Rubiadin Mediates the Upregulation of Hepatic Hepcidin and Alleviates Iron Overload via BMP6/SMAD1/5/9-Signaling Pathway. Int J Mol Sci. 2025;26. 10.3390/ijms26031385
- Wang S, Du R, Liu J, Zhong W, Zhang C, et al. Multi-approach analysis reveals the mechanism by which Shugan Xiaozhi decoction protects against metabolic dysfunction-associated steatohepatitis. Phytomedicine. 2025;141:156712. 10.1016/j.phymed.2025.156712
- Satehi MB, Karimi M, Eskandari A, Mahmoodi H. The effect of aqueous extract of Iranian oak () on lipid profile and liver enzymes in beta-thalassemia patients: a randomized controlled trial, double-blind, placebo-controlled. Front Nutr. 2025;12:1537420. 10.3389/fnut.2025.1537420
- Chen W, He C, Wen B, Sun H, Yang X, et al. [Biejiajian Pill Regulates Ferroptosis in Hepatocellular Carcinoma Cells via p62/Keap1/NRF2 Signaling Pathway: A Mechanism Study]. Sichuan Da Xue Xue Bao Yi Xue Ban. 2025;56:51. 10.12182/20250160502
- Li Y, Zhao M, Liu Y, Wang L, Huang Y, et al. 46, XY disorders of sex development combined with aceruloplasminaemia: a case report and review of the literature. Orphanet J Rare Dis. 2025;20:124. 10.1186/s13023-025-03626-2
- Zhai S, Yang Y, Zhou Y, Lai Q, Li K, et al. -Induced Liver Damage Through Ferroptosis in Rat Model. Cells. 2025;14. 10.3390/cells14050328
Data last updated:
