Rhizoma Chuanxiong comes from the plant Ligusticum chinensis.Chuan Xiong,-MW4801sf- unsulfured herb Ligusticum chuanxiong rhizome Ligusticum / Szechuan lovage rhizome<- The herb is available for sale at places like Amazon.
"Tetramethylpyrazine (TMP) is the major bioactive constituent of Rhizoma Chuanxiong which has long been used as an important component in several Chinese medicine formulations. We investigated the cellular effects of TMP in cultured primary chondrocytes. Chondrocytes isolated from the knee articular cartilage of SD rats were cultured and identified using toluidine blue staining. The second generation of chondrocytes was treated with or without TMP. TMP treatment could promote chondrocyte proliferation via pushing the progression of cell cycle. the mRNA and protein levels of Cyclin D1 and CDK4 were significantly enhanced after TMP treatment[this could apply to MSCs as well and to growth plate chondrocytes, it depends whether TMP enhances Cyclin D1 via Beta-Catenin to how effective it is though], whereas those of p21 were significantly decreased."
"G1/S transition, which is one of the two main checkpoints, is a rate-limiting step in the cell cycle and regulates the cell proliferation. G1/S progression is highly regulated by Cyclin D1 and Cyclin-dependent kinase 4 (CDK4). Cyclin D1, which is the first cyclin produced in the cell cycle, binds to existing CDK4, forming the active Cyclin D1-CDK4 complex, which in turn phosphorylates the retinoblastoma susceptibility protein (Rb). The phosphorylated Rb dissociates from the E2F/DP1/Rb complex, activating E2F. Activation of E2F{a couple E2F forms were downregulated by LSJL} results in transcription of various genes, such as Cyclin E and Cyclin A, regulating other cell cycle phases. p21 is a inhibitory protein of cell cycle, which prevents cell cycle progression by binding to and inactivating, Cyclin D1-CDK4 complex[so inhibiting p21 is another potential method to grow taller and TMP inhibits p21]."
TMP should increase chondrocyte hypertrophy as well and thus also adult height but since they were studying osteoarthritis they were likely not interested in this effect.
The Study Effects of tetramethylpyrazine on nitric oxide/cGMP signaling after cerebral vasospasm in rabbits. suggests that the effects of TMP involve NO/cGMP which would mean the effects of TMP are partially Beta-Catenin dependent. And too much Beta-Catenin can result in apoptosis. However the decrease of p21 may be independent of Beta-Catenin.
However in the study The protective effect of tetramethylpyrazine on cartilage explants and chondrocytes., no apoptotic effects were found on chondrocytes at 200 microM of TMP.
In the study Alleviation of CCl4-induced cirrhosis in rats by tetramethylpyrazine is associated with downregulation of leptin and TGF-beta1 pathway., TMP was found to downregulate the TGF-Beta1 and leptin pathways. TGF-Beta1 increases Sox9 thus decreasing Beta-Catenin. Thus TMP may upregulate Beta-Catenin in this and this increases Cyclin D1. Leptin stimulates MAPK pathway. MAPK pathway antagonizes the formulation of the Beta-Catenin/LEF complex. Since TMP downregulates the Leptin pathway, TMP increases the formation of the Beta-Catenin/LEF complex thus increasing Cyclin D1 levels.
Thus, the effects on Cyclin D1 by TMP are likely mediated by Beta-Catenin which makes it a less promising treatment than Beta-Catenin independent methods.
According to the study Wnt/β-catenin signaling induces the aging of mesenchymal stem cells through the DNA damage response and the p53/p21 pathway., Beta-Catenin signaling increases p21 levels that means that effects of TMP on p21 are likely Beta-Catenin independent so it may be worth taking a supplement that contains TMP for that effect.
So it's worth taking TMP to decrease p21 levels independent of Beta-Catenin signaling.
TMP decreases TGF-Beta1 and Leptin pathways. Thus you would want to compensate by stimulating those pathways you can take Leptin and increase TGF-Beta1 via LSJL and other supplements. TMP also stimulates the NO pathway which stimulates cGMP which decreases FGFR3 which inhibits cyclin D1 expression. So in this way TMP increases Cyclin D1 independently of Beta-Catenin.
So TMP is a worthwhile supplement but you'll want to take Leptin & TGF-Beta1 supplements to keep Beta-Catenin in check.
"G1/S transition, which is one of the two main checkpoints, is a rate-limiting step in the cell cycle and regulates the cell proliferation. G1/S progression is highly regulated by Cyclin D1 and Cyclin-dependent kinase 4 (CDK4). Cyclin D1, which is the first cyclin produced in the cell cycle, binds to existing CDK4, forming the active Cyclin D1-CDK4 complex, which in turn phosphorylates the retinoblastoma susceptibility protein (Rb). The phosphorylated Rb dissociates from the E2F/DP1/Rb complex, activating E2F. Activation of E2F{a couple E2F forms were downregulated by LSJL} results in transcription of various genes, such as Cyclin E and Cyclin A, regulating other cell cycle phases. p21 is a inhibitory protein of cell cycle, which prevents cell cycle progression by binding to and inactivating, Cyclin D1-CDK4 complex[so inhibiting p21 is another potential method to grow taller and TMP inhibits p21]."
TMP should increase chondrocyte hypertrophy as well and thus also adult height but since they were studying osteoarthritis they were likely not interested in this effect.
The Study Effects of tetramethylpyrazine on nitric oxide/cGMP signaling after cerebral vasospasm in rabbits. suggests that the effects of TMP involve NO/cGMP which would mean the effects of TMP are partially Beta-Catenin dependent. And too much Beta-Catenin can result in apoptosis. However the decrease of p21 may be independent of Beta-Catenin.
However in the study The protective effect of tetramethylpyrazine on cartilage explants and chondrocytes., no apoptotic effects were found on chondrocytes at 200 microM of TMP.
In the study Alleviation of CCl4-induced cirrhosis in rats by tetramethylpyrazine is associated with downregulation of leptin and TGF-beta1 pathway., TMP was found to downregulate the TGF-Beta1 and leptin pathways. TGF-Beta1 increases Sox9 thus decreasing Beta-Catenin. Thus TMP may upregulate Beta-Catenin in this and this increases Cyclin D1. Leptin stimulates MAPK pathway. MAPK pathway antagonizes the formulation of the Beta-Catenin/LEF complex. Since TMP downregulates the Leptin pathway, TMP increases the formation of the Beta-Catenin/LEF complex thus increasing Cyclin D1 levels.
Thus, the effects on Cyclin D1 by TMP are likely mediated by Beta-Catenin which makes it a less promising treatment than Beta-Catenin independent methods.
According to the study Wnt/β-catenin signaling induces the aging of mesenchymal stem cells through the DNA damage response and the p53/p21 pathway., Beta-Catenin signaling increases p21 levels that means that effects of TMP on p21 are likely Beta-Catenin independent so it may be worth taking a supplement that contains TMP for that effect.
So it's worth taking TMP to decrease p21 levels independent of Beta-Catenin signaling.
TMP decreases TGF-Beta1 and Leptin pathways. Thus you would want to compensate by stimulating those pathways you can take Leptin and increase TGF-Beta1 via LSJL and other supplements. TMP also stimulates the NO pathway which stimulates cGMP which decreases FGFR3 which inhibits cyclin D1 expression. So in this way TMP increases Cyclin D1 independently of Beta-Catenin.
So TMP is a worthwhile supplement but you'll want to take Leptin & TGF-Beta1 supplements to keep Beta-Catenin in check.
Couldn't find any specific anti-bone effects.
DO You know an any method to grow up after the grow plates are closed? ( i hate it..)
ReplyDeleteI wanted to ask, lets suppose we had developed a method to inject stem cells into a growth plate near a joint and it works, how many growth plates are there total in the human body? would we have to inject into all of them for proportional growth? is that correct? the shoulders, the rib cage?
ReplyDeletedo they contain growth plates also?
be sure to backup your entire blog unto a hardrive
ReplyDelete