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Pharmacological acceleration of mammary gland involution in cows.

机译:母牛乳腺退化的药理作用加速。

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Mammary gland involution is a compound physiological process that is characterized by differentiation and apoptosis of mammary epithelial cells. Involution is controlled by prolactin, growth hormones, oestrogens, progesterone, cortisol and insulin-like growth factor 1 (IGF-1). Advanced pregnancy, infrequent milking, and mastitis increase epithelial cell apoptosis. Milk stasis triggers local stimuli which cause the leak-tight junctions and initiate involution. Cows are especially susceptible to intramammary infections (IMI) by contagious pathogens during the dry period and environmental pathogens during parturition. High milk yield during the dry period is a significant risk factor for the cows and udder quarters are usually infected with environmental pathogens during calving. It is observed that high producing cows rarely develop a keratin plug which is the natural protection against infection during dry period. Milk production has to be reduced in these high producing cows during the dry period either by restricted diet, interrupted milking or pharmacological treatment. It is also noted that intramammary infusion of colchicine and endotoxin during dry period accelerates mammary involution. Infusion of ConA or PHA near the dry period also accelerates mammary involution resulting in elevated levels of natural protective factors. Interleukin-2 accelerates involution and stimulates local antibody production more than pokeweed mitogen and LPS. Intramammary infusion of either rboGm-CSF or rboII-1 beta at the cessation of milking immediately increases the number of phagocytic cells in the mammary glands. These cytokines, particularly rboII-1 beta , can increase the rate of mammary gland involution. The infusion of beta 1.3-glucan during the dry period accelerates the involution process by increasing the somatic cells, particularly the number of macrophages in the milk. Casein hydrolysates are among the milk-borne factors that cause the disruption of tight junction integrity and induce involution in cows. Mammary tissue involution is affected by exogenous oestrogen through the activation of plasminogen. Endogenous oestrogen secreted by the developing fetus and placenta may partially mediate the gradual involution that occurs during lactation..
机译:乳腺退化是一个复合的生理过程,其特征在于乳腺上皮细胞的分化和凋亡。退化受催乳素,生长激素,雌激素,孕酮,皮质醇和胰岛素样生长因子1(IGF-1)的控制。妊娠晚期,不频繁挤奶和乳腺炎会增加上皮细胞凋亡。牛奶淤滞会触发局部刺激,从而引起密封连接并引发内卷。奶牛在干燥期特别容易受到传染性病原体在分娩期间发生环境内病原体感染的感染。干旱时期的高产牛奶是奶牛的重要危险因素,在产犊期间,乳房区通常会感染环境病原体。观察到高产奶牛很少会形成角蛋白栓,这是干燥期间抵抗感染的天然保护。在干燥时期,必须通过限制饮食,中断挤奶或药物治疗来减少这些高产奶牛的产奶量。还应注意的是,干燥期间在乳房内注入秋水仙碱和内毒素会加速乳房退化。在干燥期附近注入ConA或PHA也会加速乳腺退化,导致自然保护因子水平升高。与商陆有丝分裂原和LPS相比,白介素2加速了内卷化并刺激了局部抗体的产生。停止挤奶后,在乳腺内注入rboGm-CSF或rboII-1 beta会立即增加乳腺中吞噬细胞的数量。这些细胞因子,特别是rboII-1 beta,可以增加乳腺退化的速度。在干燥时期输注β1.3-葡聚糖可通过增加体细胞,特别是牛奶中巨噬细胞的数量来加速对合过程。酪蛋白水解物是牛奶传播的因素之一,其导致紧密连接完整性的破坏并引起母牛的退化。乳腺组织的退化受纤溶酶原的激活而受外源雌激素的影响。发育中的胎儿和胎盘分泌的内源性雌激素可能部分介导泌乳过程中发生的逐渐退化。

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