Condition
Bladder Cancer
Bladder cancer begins when cells in the bladder lining grow out of control, with smoking as the leading risk factor. Vitamin D has the strongest support among supplements, rated moderate, with low levels linked to bladder cancer outcomes, while green tea extract is limited, backed mainly by studies linking green tea to lower risk. Salidroside slowed bladder cancer cells in a lab dish, but that work has no human confirmation.
Sources: PMID 21520297
- Supplements studied
- 1
- Graded outcomes
- 1
Evidence by supplement
- Strong
- Moderate
- Limited
- Very limited
| Grade | Outcome | Effect | Size | Studies | People | Studies list |
|---|---|---|---|---|---|---|
| Bladder Cancer Cell Growth In vitro, Rhodiola rosea extracts and salidroside decreased bladder cancer cell line growth via inhibition of the mTOR pathway and induction of autophagy. This is limited to a single cell-line study with no animal or human confirmation. | Improves (the measure goes down) | Small effect | 5 studies | |||
Studies that measured bladder cancer cell growth | ||||||
Key findings
- Bladder Cancer Cell GrowthImproves (the measure goes down)
The Bladder Cancer Supportive Care protocol
2 primary supplements · 6 supporting supplements
- Vitamin D2,000–4,000 IU daily (target 40–60 ng/mL)
- Green Tea Extract (EGCG)250–500 mg EGCG daily
Studies cited
23 studies from PubMed
- Salidroside directly activates HSC70, revealing a new role for HSC70 in BDNF signalling and neurogenesis after cerebral ischemia.
- Salidroside pretreatment alleviates PM2.5 caused lung injury via inhibition of apoptosis and pyroptosis through regulating NLRP3 Inflammasome.
- Network pharmacology analysis combined with experimental validation to explore the therapeutic mechanism of salidroside on intestine ischemia reperfusion.
- Salidroside Attenuates Airway Inflammation and Remodeling via the miR-323-3p/SOCS5 Axis in Asthmatic Mice.
- Salidroside Exerts Beneficial Effect on Testicular Ischemia-Reperfusion Injury in Rats.
- Safety of a Sustainably Produced, Bioengineered, Nature-Identical Salidroside Compound.
- Salidroside in the Treatment of NAFLD/NASH.
- Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy.
- The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside via regulating the PTEN mediated PI3K/Akt/NF-κB signaling pathway.
- Contribution of salidroside to the relieve of symptom and sign in the early acute stage of osteoarthritis in rat model.
- Salidroside Alleviates Cartilage Degeneration Through NF-κB Pathway in Osteoarthritis Rats.
- Salidroside inhibits platelet function and thrombus formation through AKT/GSK3β signaling pathway.
- Salidroside as a potential neuroprotective agent for ischemic stroke: a review of sources, pharmacokinetics, mechanism and safety.
- Salidroside Inhibits Lipopolysaccharide-ethanol-induced Activation of Proinflammatory Macrophages via Notch Signaling Pathway.
- Salidroside inhibits inflammatory factor release in BV-2 cells through p38 and JNK pathways.
- Salidroside protects against kainic acid-induced status epilepticus via suppressing oxidative stress.
- Salidroside, a Bioactive Compound of Rhodiola Rosea, Ameliorates Memory and Emotional Behavior in Adult Mice.
- Salidroside exhibits anti-dengue virus activity by upregulating host innate immune factors.
- Salidroside protects Caenorhabditis elegans neurons from polyglutamine-mediated toxicity by reducing oxidative stress.
- Antidepressant-like effects of salidroside on olfactory bulbectomy-induced pro-inflammatory cytokine production and hyperactivity of HPA axis in rats.
- Salidroside attenuates LPS-stimulated activation of THP-1 cell-derived macrophages through down-regulation of MAPK/NF-kB signaling pathways.
- Rhodiola rosea extracts and salidroside decrease the growth of bladder cancer cell lines via inhibition of the mTOR pathway and induction of autophagy.
- Salidroside and tyrosol from Rhodiola protect H9c2 cells from ischemia/reperfusion-induced apoptosis.