Fibrosis Leads to Destruction of Hair Follicles in Advanced cases of MPB
Fibrosis was identified several years back as a causative factor in Androgenetic hair loss by L'Oreal, who patented a treatment that consisted of Green Tea Extract, Grape Seed Extract, and Taurine, called Hair Mass. This is a recent study that corroborates their findings. Even though Hair Mass was marketed for women's hair loss the feedback on its effectiveness from both genders using it for 3 months or more has been uniformly positive.
The supplement taurine, has been well documented as a potent systemic anti-fibrotic agent , and has demonstrated anti-fibotic effects in various sites and organs in every study done thus far. L'OReal's findings, that the combination of Taurine/Green Tea/Grape Seed /Zinc effectively countered fibrosis of the hair follicle and thus treated hair loss in women comes as no surprise.
Androgenetic alopecia in males: a histopathological and ultrastructural study
J Cosmet Dermatol. 2009 Jun;8(2):83-91
Androgenetic alopecia in males: a histopathological and ultrastructural study.
El-Domyati M, Attia S, Saleh F, Abdel-Wahab H.
Department of Dermatology, Faculty of Medicine, Al-Minya University, Al-Minya, Egypt.
Background Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process. Aims To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (AGA). Patients/methods Fifty-five subjects were included in this study (40 with AGA and 15 as normal age-matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study. Results The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases. Conclusion Follicular microinflammation plays an integral role in the pathogenesis of AGA in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases.
Mast Cells are also implicated in the development of fibrosis associated with the hair follicle destruction seen in MPB. Mast cell induced histamine release can be effectively countered with the use of Curcumin. Curcumin can also effectively inhibit fibrosis by the down-regulation of tgf beta.
Curcumin inhibits Histamine Release from Mast Cells
Biological & Pharmaceutical Bulletin
Vol. 32 (2009) , No. 5 842
Effects of Analogues of Curcumin on Histamine Release from Mast Cells
Curcumin reportedly has anti-allergenic effects can inhibit the release of histamine from mast cells. In the present study, fourteen benzylidenecyclopentanone analogues of curcumin were studied for their effects on histamine release from rat basophilic leukemia (RBL-2H3) cells. After screening, four selected compounds: 2,5-bis(4-hydroxybenzylidene)cyclopentanone; 2,5-bis(4-hydroxy-3-methoxybenzylidene)cyclopentanone; 2,5-bis(4-hydroxy-3,5-dimethylbenzylidene) cyclopentanone; and 2,5-bis(4-hydroxy-3,5-diethylbenzylidene)cyclopentanone were studied for their concentration-dependent effects on histamine release and Ca2+ uptake. In RBL-2H3 cells and rat peritoneal mast cells stimulated with antigen or compound 48/80, respectively, the methoxy-hydroxy analogue was more potent than curcumin in inhibiting histamine release. In contrast, the inhibitory effects of methyl/ethyl analogues were less potent than those of curcumin. Moreover, these compounds abrogated histamine release induced by increased intracellular Ca2+ concentrations in response to stimulants such as thapsigargin and ionomycin. These compounds also showed potent inhibitory effects on 45Ca2+ uptake in RBL-2H3 cells. The mechanism of the inhibitory effects of these curcumin analogues on histamine release appeared to be related to blockade of Ca2+ signaling events. These results provide useful information to guide the development of new synthetic compounds for the treatment of allergic and inflammatory diseases related to histamine or mast cells.
Effects of curcumin on TNF-alpha and TGF-beta1 in serum in mice
CausticSymmetry on Thu May 14, 2009
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009 May;25(5):399-401.
[Effects of curcumin on TNF-alpha and TGF-beta1 in serum and lung tissue of SiO(2);-induced fibrosis in mice.]
[Article in Chinese]
Jiang ZY, Zou L, Shi SS, Lu YR, Dong J, Yang CH, Lu YC, Dai GK.
Department of Microbiology and Immunology, Medical College, Jinan University, Guangzhou 510632, China.
AIM: To study the effects of curcumin on TNF-alpha and TGF-beta1 in serum and lung tissue of SiO(2);-induced fibrosis in mice. METHODS: 75 mice were divided into five groups. After treated with curcumin 6 and 9 mice of each group were sacrificed on day 14 and 42 respectively to take their blood and lung tissue. The level of TNF-alpha and TGF-beta1 was observed by ELISA. RESULTS: The infection reaction of lung tissue and fibrosis in model group was obvious. Compared with sham operation group, TNF-alpha and TGF-beta1 in serum and lung tissue increased significantly(P<0.01), but decreased in different degrees after treated with curcumin(P<0.05). CONCLUSION: Curcumin can decrease the level of TNF-alpha and TGF-beta1 in serum and lung tissue of SiO(2);-induced fibrosis in mice and have the anti-fibrosis role by deregulating cytokine level.
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