I've been using an alcohol ginger extract on my scalp as well as clobetasol, tricomin and a salicylic acid shampoo called Sebulex. I'm getting a lot of dark tiny hairs (not vellus crap that only looks dark depending on the lighting angle). The addition of the ginger extract has kicked things into gear. What do you guys think of it in a regimen? I originally wanted it as I saw it mentioned as a PGD2 inhibitor. Some additional info about ginger:
"Through screening a wide variety of oriental pharmaceuticals for inducing IGF-1, Phlomis umbrosa Turez, Cynanchumwilfordii(Max) Hem&ley, Zingiber Officinale Rosc. and Platycodi Radix have been proved to exhibit considerable ability to induce IGF-1."
"The aim of the present study was to determine the effect of ginger extract on macrophage activation and APC function. Our results indicate that ginger extract inhibits LPS induced activation of macrophages by inhibiting the proinflammatory cytokine and chemokine release and decreasing the costimulatory molecule expression. Our results support the previous studies that reported the suppressive effect of ginger extract on expression of pro-inflammatory genes [7]. It can be concluded from our data as well as the previous reports that ginger extract inhibits pro inflammatory cytokine release by macrophages irrespective of the monocyte heterogeneity.
Our results also indicate that GE inhibits macrophage activation leading to decrease in T cell proliferation in response to alloantigen. We observed an inhibition of proinflammatory cytokine release by ginger extract treated macrophages. In addition we observed a decrease in costimulatory molecule expression on ginger extract treated macrophages. Further ginger extract also decreased the MHC II expression on LPS activated macrophages. The functional consequence of the inhibitory effect of ginger extract on macrophages was seen in form of decrease in T cell proliferation in the primary MLR. This is further supported by decreased production of IL-2 and IFN-? in the primary MLR containing ginger extract treated macrophages as APCs. Ginger is known to be anti-inflammatory in nature but its mechanism of action is not completely known. Our study for the first time shows the mechanism by which ginger exerts its anti inflammatory effects on macrophage and T cell activation. Ginger extract not only inhibits proinflammatory cytokine production by macrophages but also decreases IFN-? production, the key pro inflammatory mediator, by T cells.
LPS is an important activating stimulus. LPS stimulation leads to an effective classical macrophage activation [12,13]. Classically activated macrophages are highly pro inflammatory and they secrete IL-12. In the presence of IL-12 a Th1 response predominates. Activated Th1 cells produce IFN-?, which initiates a positive feedback loop by priming and activating more macrophages and by upregulating their MHC class II expression. IFN-? also acts synergistically with TNF-? in macrophage activation initiating three different signalling arms viz., 1) FADD-dependent binding and activation of caspase-8, 2) activation of JNK pathway and 3) activation of NF?B. IL-1? also plays a role in macrophage activation [13,14]. Binding of IL-1? to IL-1R1 activates both MAPK-AP1 and I-?B kinase-NF?B pathways. Ginger extract exerts an inhibitory effect on the production of IL-12 thereby indirectly suppressing the production of IFN-? and its positive feedback loop of macrophage activation. Inhibition of macrophage activation is further enhanced by a drastic decrease in TNF-? production along with inhibition of IL-1? production.
In addition to inhibition of macrophage activation ginger extract also negatively affects monocyte and leukocyte migration as evident from inhibition of RANTES and MCP-1 production. Increase RANTES production is associated with a wide range of inflammatory disorders. It acts by promoting leukocyte infiltration to the site of inflammation. At high concentrations RANTES induces activation of T cells in a manner not dissimilar to mitogens [15]. The activation of T cells by RANTES is followed by increased production of IL-2 and IFN-?. Inhibition of RANTES production by ginger extract not only suppresses inflammation, but also restricts T cell activation, as observed by decreased IFN-? production (Fig. 5). MCP-1 is a pro inflammatory cytokine responsible in the appearance of a monocyte rich inflammatory infiltrate [16]. Ginger extract inhibits the production of MCP-1 completely indicating an inhibition of macrophage activation.
The classically activated macrophages play a role as effector cells in Th1 cellular response by upregulating surface molecules like MHC class II and B7. Ginger extract down regulates the expression of both MHC class II and B7 molecules as shown in Figure 2 and 3. This in turn inhibits the activation of CD4+ T lymphocytes which is evident from decreased IFN-? production (Fig. 5) and also inhibition of CD4+ T lymphocyte proliferation in response to alloantigen (Fig. 4).
The present study confirms the inhibitory effect of ginger extract on production of proinflammatory cytokines as shown by previous studies. In addition it demonstrates a novel inhibitory property of ginger. The inhibition of costimulatory molecule and MHC class II molecules by ginger extract suggests that ginger has inhibitory effect on macrophage maturation, activation as well as on its APC function. Antigen presentation by MHC class II molecules alongwith the costimulatory signal are both necessary to initiate an effective T cell activation. A decrease in the expression of either or both fails to bring about T cell activation followed by proliferation. We show an inhibitory effect of ginger on T cell proliferation which is an indirect effect mediated by inhibition of macrophage activation. Inhibition of T cell activation and proliferation is also indicated by a low IL-2 and IFN-? production."
I'm pretty interested in Gingers ability to inhibit MHC Class II, as it has been posted on this site before:
"CD200 was downregulated in follicles from balding areas. Along with an upregulation of MHC1 and MHC2 markers on these follicles it seems that they are marked as potential dangers for the immune system."
I think that on top of this, local scalp flora can enhance inflammation and think that inhibiting MHC Class II might help there as for example Staph superantigens bind to MHC Class II on antigen presenting cells and produce large amounts of pro-inflammatory cytokines.
"Through screening a wide variety of oriental pharmaceuticals for inducing IGF-1, Phlomis umbrosa Turez, Cynanchumwilfordii(Max) Hem&ley, Zingiber Officinale Rosc. and Platycodi Radix have been proved to exhibit considerable ability to induce IGF-1."
"The aim of the present study was to determine the effect of ginger extract on macrophage activation and APC function. Our results indicate that ginger extract inhibits LPS induced activation of macrophages by inhibiting the proinflammatory cytokine and chemokine release and decreasing the costimulatory molecule expression. Our results support the previous studies that reported the suppressive effect of ginger extract on expression of pro-inflammatory genes [7]. It can be concluded from our data as well as the previous reports that ginger extract inhibits pro inflammatory cytokine release by macrophages irrespective of the monocyte heterogeneity.
Our results also indicate that GE inhibits macrophage activation leading to decrease in T cell proliferation in response to alloantigen. We observed an inhibition of proinflammatory cytokine release by ginger extract treated macrophages. In addition we observed a decrease in costimulatory molecule expression on ginger extract treated macrophages. Further ginger extract also decreased the MHC II expression on LPS activated macrophages. The functional consequence of the inhibitory effect of ginger extract on macrophages was seen in form of decrease in T cell proliferation in the primary MLR. This is further supported by decreased production of IL-2 and IFN-? in the primary MLR containing ginger extract treated macrophages as APCs. Ginger is known to be anti-inflammatory in nature but its mechanism of action is not completely known. Our study for the first time shows the mechanism by which ginger exerts its anti inflammatory effects on macrophage and T cell activation. Ginger extract not only inhibits proinflammatory cytokine production by macrophages but also decreases IFN-? production, the key pro inflammatory mediator, by T cells.
LPS is an important activating stimulus. LPS stimulation leads to an effective classical macrophage activation [12,13]. Classically activated macrophages are highly pro inflammatory and they secrete IL-12. In the presence of IL-12 a Th1 response predominates. Activated Th1 cells produce IFN-?, which initiates a positive feedback loop by priming and activating more macrophages and by upregulating their MHC class II expression. IFN-? also acts synergistically with TNF-? in macrophage activation initiating three different signalling arms viz., 1) FADD-dependent binding and activation of caspase-8, 2) activation of JNK pathway and 3) activation of NF?B. IL-1? also plays a role in macrophage activation [13,14]. Binding of IL-1? to IL-1R1 activates both MAPK-AP1 and I-?B kinase-NF?B pathways. Ginger extract exerts an inhibitory effect on the production of IL-12 thereby indirectly suppressing the production of IFN-? and its positive feedback loop of macrophage activation. Inhibition of macrophage activation is further enhanced by a drastic decrease in TNF-? production along with inhibition of IL-1? production.
In addition to inhibition of macrophage activation ginger extract also negatively affects monocyte and leukocyte migration as evident from inhibition of RANTES and MCP-1 production. Increase RANTES production is associated with a wide range of inflammatory disorders. It acts by promoting leukocyte infiltration to the site of inflammation. At high concentrations RANTES induces activation of T cells in a manner not dissimilar to mitogens [15]. The activation of T cells by RANTES is followed by increased production of IL-2 and IFN-?. Inhibition of RANTES production by ginger extract not only suppresses inflammation, but also restricts T cell activation, as observed by decreased IFN-? production (Fig. 5). MCP-1 is a pro inflammatory cytokine responsible in the appearance of a monocyte rich inflammatory infiltrate [16]. Ginger extract inhibits the production of MCP-1 completely indicating an inhibition of macrophage activation.
The classically activated macrophages play a role as effector cells in Th1 cellular response by upregulating surface molecules like MHC class II and B7. Ginger extract down regulates the expression of both MHC class II and B7 molecules as shown in Figure 2 and 3. This in turn inhibits the activation of CD4+ T lymphocytes which is evident from decreased IFN-? production (Fig. 5) and also inhibition of CD4+ T lymphocyte proliferation in response to alloantigen (Fig. 4).
The present study confirms the inhibitory effect of ginger extract on production of proinflammatory cytokines as shown by previous studies. In addition it demonstrates a novel inhibitory property of ginger. The inhibition of costimulatory molecule and MHC class II molecules by ginger extract suggests that ginger has inhibitory effect on macrophage maturation, activation as well as on its APC function. Antigen presentation by MHC class II molecules alongwith the costimulatory signal are both necessary to initiate an effective T cell activation. A decrease in the expression of either or both fails to bring about T cell activation followed by proliferation. We show an inhibitory effect of ginger on T cell proliferation which is an indirect effect mediated by inhibition of macrophage activation. Inhibition of T cell activation and proliferation is also indicated by a low IL-2 and IFN-? production."
I'm pretty interested in Gingers ability to inhibit MHC Class II, as it has been posted on this site before:
"CD200 was downregulated in follicles from balding areas. Along with an upregulation of MHC1 and MHC2 markers on these follicles it seems that they are marked as potential dangers for the immune system."
I think that on top of this, local scalp flora can enhance inflammation and think that inhibiting MHC Class II might help there as for example Staph superantigens bind to MHC Class II on antigen presenting cells and produce large amounts of pro-inflammatory cytokines.