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Aegis 120 Caps

Aegis 120 Caps
Brand: Antaeus Labs
Product Code: P2439
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Availability: In Stock
Price: £39.66
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Description

Antaeus Labs AEGIS 120 Caps Description

Description

  • State of the art liver cleansing agent
  • AEGIS is a unique compound which no other company has produced
  • Antaeus Labs AEGIS is designed to be used during prohormone use and after, during PCT
  • No other liver protection agent comes close to AEGIS for preventing liver toxicity
  • The best liver support supplement

 

Review

If you´re looking for a comprehensive liver support product then look no further than Aegis by Anataeus Labs. Aegis is a unique compound designed to protect the liver during prohormone cycles. Run your prohormone cycle safe in the knowledge that you have one of the best possible liver support products available.

 

Antaeus Labs AEGIS Description

There are numerous sources of liver damage, but only one associated with the use of oral prohormones or anabolic steroids -- cholestasis. Cholestasis is defined as a failure of bile to reach the duodenum, which could be due to a number of different pathological states between the hepatocyte and the ampulla of Vater. When somebody takes oral prohormones (especially 17-AA ones) the physical structure of the hepatocyte is changed -- microfilaments and canaliculi become less contractile. Changes in the canalicular bile salt export pump may also occur. This leads to decreased bile flow and the retention of highly toxic hydrophobic bile salts. At low levels, these bile salts cause apoptosis; at higher concentrations, tissue death and serious liver damage.

This is where AEGIS comes into the picture. It was designed with users of oral prohormones in mind, and brings together the best anti-cholestatic nutrients bar none.

Tauroursodeoxycholic acid:
-Can stop apoptosis during cholestasis. Toxic bile acids produce apoptosis Via fas- and TRAIL- death receptor mediated pathways. Both are, to some degree, dependent on the translocation of the ´bax´ pro-apoptoic molecule from the cytosol of hepatocytes to the cell mitochondria. TUDCA prevents bax translocation, strongly stabilizes mitochondrial membranes, and activates the MAPK pro-survival pathway in hepatocytes. (1) These effects protect hepatocytes from bax-related apoptosis.
-Is a hydrophilic bile acid, and its presence markedly shifts the bile pool towards hydrophilicity, which, to some extent, detoxifies it. When used consistently, especially at pharmacological doses, TUDCA (along with UDCA) eventually becomes the predominant bile acid in the liver and in general circulation. (2)
-Directly stimulates bile secretion via modulating cellular signalling pathways in hepatocytes, such as ERK, src, PKC and others. These signalling pathways generally phosphorylate, or activate, the bile salt export pump (BSEP) and other processes involved in bile export/secretion. (For example, PKC-alpha-mediated secretion of HCO3-.) (3, 4, 5)

Polyenylphosphatidylcholine:
-Stabilizes cellular membranes and dilates bile canaliculi. This former effect has been shown to protect human cells from hydrophobic bile salt induced apoptosis (6), and the latter may serve to counteract the reduction in contractility seen in androgen-induced cholestasis. (7)
-Oral androgen administration may decrease hepatic Na+, K+-ATPase, Ca2+, Mg2+-ATPase and F-actin levels --- all of which may be restored, and even raised, by polyenylphosphatidylcholine administration. (8)
-Is secreted into bile by hepatocytes, where it serves as a major component of the micelles in which bile acids are emulsified. Increased levels of biliary phosphatidylcholine reduces the cytotoxicity of bile acids, whereas phosphatidylcholine-secretion impairment (as is often seen in ABCB4 disease) is characterized by extremely severe cholestatic liver disease. (9)

To summarize: Aegis is highly-potent, highly-specific liver protection supplements for people taking hepatotoxic oral androgens. Superior protection cannot be bought, nor should it be needed.

References:
1. Joana D. Ameral, Ricardo J. S, Viana, Rita M. Ramalho, Clifford J. Steer, and Cec

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