关于Lactoferrin,看看到底是桂鸣对还是方舟子对?(ZT)


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送交者: USTC3 于 2007-03-29, 15:09:08:

回答: 无耻 由 方舟子 于 2007-03-29, 12:11:23:

方舟子说:

引用:
lactoferrin(乳铁蛋白)不是激素,而是一种由多达703个氨基酸
组成的大蛋白质,在消化道中被消化降解成lactoferrcin
(乳铁蛋白肽),在肠道中发挥抗细菌、病毒的作用,但是
从未见到它还能跑到体内增强骨质的专业报道。

桂鸣说:

引用:
牛奶人奶当中有calcitonin, lactoferrin这样的蛋白肽类激素物质,对促进成骨细胞的活性,抑制破骨细胞的活性,提高骨密质,减少骨质疏松有明显的作用。新生儿通过吸收母乳中的多种生长激素,不仅促进生长发育,也提高抵御疾病的能力。这是人工配方的奶粉所无法达到的。成年人对蛋白肽类的直接吸收能力较新生儿大大减弱,但也不一定完全不能吸收,因为激素类物质只要很低的浓度就可以发挥显著的作用。而且,吸收不一定要从肠道开始。口腔粘膜就可以直接吸收一些激素类蛋白肽。从研究来看,不同种类动物的lactoferrin可以交叉起作用。

引用:
Endocrinology. 2004 Sep;145(9):4366-74. Epub 2004 May 27.

Lactoferrin is a potent regulator of bone cell activity and increases bone
formation in vivo.

Cornish J, Callon KE, Naot D, Palmano KP, Banovic T, Bava U, Watson M, Lin JM,
Tong PC, Chen Q, Chan VA, Reid HE, Fazzalari N, Baker HM, Baker EN, Haggarty NW,
Grey AB, Reid IR.

Department of Medicine, University of Auckland, Private Bag 92019, Auckland
1001, New Zealand. j.cornish@auckland.ac.nz.

Lactoferrin is an iron-binding glycoprotein present in epithelial secretions,
such as milk, and in the secondary granules of neutrophils. We found it to be
present in fractions of milk protein that stimulated osteoblast growth, so we
assessed its effects on bone cell function. Lactoferrin produced large,
dose-related increases in thymidine incorporation in primary or cell line
cultures of human or rat osteoblast-like cells, at physiological concentrations
(1-100 microg/ml). Maximal stimulation was 5-fold above control. Lactoferrin
also increased osteoblast differentiation and reduced osteoblast apoptosis by up
to 50-70%. Similarly, lactoferrin stimulated proliferation of primary
chondrocytes. Purified, recombinant, human, or bovine lactoferrins had similar
potencies. In mouse bone marrow cultures, osteoclastogenesis was
dose-dependently decreased and was completely arrested by lactoferrin, 100
microg/ml, associated with decreased expression of receptor activator of nuclear
factor-kappaB ligand. In contrast, lactoferrin had no effect on bone resorption
by isolated mature osteoclasts. Lactoferrin was administered over calvariae of
adult mice for 5 d. New bone formation, assessed using fluorochrome labels, was
increased 4-fold by a 4-mg dose of lactoferrin. Thus, lactoferrin has powerful
anabolic, differentiating, and antiapoptotic effects on osteoblasts and inhibits
osteoclastogenesis. Lactoferrin is a potential therapeutic target in bone
disorders such as osteoporosis and is possibly an important physiological
regulator of bone growth.

引用:
Clin Med Res. 2005 May;3(2):93-101.

Lactoferrin--a novel bone growth factor.

Naot D, Grey A, Reid IR, Cornish J.

Department of Medicine, University of Auckland, Auckland, New Zealand.
d.naot@auckland.ac.nz

Lactoferrin is an iron-binding glycoprotein that belongs to the transferrin
family. It is present in breast milk, in epithelial secretions, and in the
secondary granules of neutrophils. In healthy subjects lactoferrin circulates at
concentrations of 2-7 x 10(-6) g/ml. Lactoferrin is a pleiotropic factor with
potent antimicrobial and immunomodulatory activities. Recently, we have shown
that lactoferrin can also promote bone growth. At physiological concentrations,
lactoferrin potently stimulates the proliferation and differentiation of primary
osteoblasts and also acts as a survival factor inhibiting apoptosis induced by
serum withdrawal. Lactoferrin also affects osteoclast formation and, in murine
bone marrow culture, lactoferrin potently inhibits osteoclastogenesis. In vivo,
local injection of lactoferrin above the hemicalvaria of adult mice results in
substantial increases in the dynamic histomorphometric indices of bone formation
and bone area. The mitogenic effect of lactoferrin in osteoblast-like cells is
mediated mainly through LRP1, a member of the family of low-density lipoprotein
receptor-related proteins that are primarily known as endocytic receptors. Using
confocal laser scanning microscopy, we demonstrated that fluorescently labeled
lactoferrin is endocytosed and can be visualized in the cytoplasm of primary
osteoblastic cells. Lactoferrin also induces activation of p42/44 MAPK signaling
in primary osteoblasts, but the two pathways seem to operate independently as
activation of MAPK signaling, but not endocytosis, is necessary for the
mitogenic effect of lactoferrin. We conclude that lactoferrin may have a
physiological role in bone growth and healing, and a potential therapeutic role
as an anabolic factor in osteoporosis.




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