Vitamin C is hepatoprotective. This review highlights the proposed methods by which vitamin C reduces ALT, AST, alkaline phosphatase, LDH, malondialdegyde...
rat model finds that progesterone effects internal cell enzyme activity. In this case, progesterone increased PP2A in the cerebellum and in the hyippocampus. Interesting, that E2 priming decreased the effects on the hippocampus, but not the cerebellum. This reveals a biochemical link between sex hormones, progesterone in this case, and the brain. Studies have shown progesterone to be neuroprotective in TBI. This may be one mechanism.
the mechanism by which PTP1B regulates adiposity and leptin sensitivity likely involves the coordinated regulation of AMPK in hypothalamus and peripheral tissues.
hyperthyroidism, whether medication induced or iatrogenic, results in elevated calcium, phosphorus, and alkaline phosphates. The T3 levels show the best correlation
The avermectins are known to possess pronounced antitumor activity
Over the past few years, there have been steadily increasing reports that ivermectin may have varying uses as an anti-cancer agent, as it has been shown to exhibit both anti-cancer and anti-cancer stem cell properties
In human ovarian cancer and NF2 tumor cell lines, high-dose ivermectin inactivates protein kinase PAK1 and blocks PAK1-dependent growth
PAK1 is essential for the growth of more than 70% of all human cancers, including breast, prostate, pancreatic, colon, gastric, lung, cervical and thyroid cancers, as well as hepatoma, glioma, melanoma, multiple myeloma and for neurofibromatosis tumors
Ivermectin suppresses breast cancer by activating cytostatic autophagy, disrupting cellular signaling in the process, probably by reducing PAK1 expression
Cancer stem cells are a key factor in cancer cells developing resistance to chemotherapies and these results indicate that a combination of chemotherapy agents plus ivermectin could potentially target and kill cancer stem cells, a paramount goal in overcoming cancer
Triple-negative breast cancers, which lack estrogen, progesterone and HER2 receptors, account for 10–20% of breast cancers and are associated with poor prognosis
Ivermectin addition led to transcriptional modulation of genes associated with epithelial–mesenchymal transition and maintenance of a cancer stem cell phenotype in triple-negative breast cancers cells, resulting in impairment of clonogenic self-renewal in vitro and inhibition of tumor growth and metastasis in vivo
Ivermectin-induced cytostatic autophagy also leads to suppression of tumor growth in breast cancer xenografts, causing researchers to believe there is scope for using ivermectin to inhibit breast cancer cell proliferation and that the drug is a potential treatment for breast cancer
ivermectin synergizes with the chemotherapy agents cytarabine and daunorubicin to induce cell death in leukemia cells
Ivermectin inhibits proliferation and increases apoptosis of various human cancers
Activation of WNT-TCF signaling is implicated in multiple diseases, including cancers of the lungs and intestine,
A new screening system has found that ivermectin inhibits the expression of WNT-TCF targets
It represses the levels of C-terminal β-catenin phosphoforms and of cyclin D1 in an okadaic acid-sensitive manner, indicating its action involves protein phosphatases
In vivo, ivermectin selectively inhibits TCF-dependent, but not TCF-independent, xenograft growth without side effects
ivermectin has an exemplary safety record, it could swiftly become a useful tool as a WNT-TCF pathway response blocker to treat WNT-TCF-dependent diseases, encompassing multiple cancers.117
In most cancers, oncogenic driver mutations such as activation of K-ras, c-Myc and phosphatidylinositol-3 (PI3) kinase or loss of phosphatase and tensin homolog (Pten) and p53, not mutations that inactivate mitochondrial respiration complexes, promote glycolysis