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       #Post#: 171--------------------------------------------------
       TUDCA
       By: Road2HardCoreIron Date: May 6, 2018, 11:40 am
       ---------------------------------------------------------
       Tauroursodeoxycholic acid (TUDCA) is an ambiphilic bile acid. It
       is the taurine conjugate form of ursodeoxycholic acid (UDCA).
       Humans are found to have trace amounts of TUDCA. However, bears
       contain large amounts of TUDCA in their bile; UDCA and
       conjugates comprise about 47% of the bile in American black
       bears and up to 76% in Asiatic bears.[1] TUDCA has been used in
       ancient Asian pharmacopoeias for its supposed beneficial
       effects. UDCA is produced in several countries for the treatment
       of gallstones and liver cirrhosis. It is not approved by the
       Food and Drug Administration, in the U.S. while UDCA is approved
       in the United States for the treatment of primary biliary
       cirrhosis[2][3] Ongoing research is finding TUDCA has
       diminishing apoptotic effects, helping with cardiac function,
       Huntington's disease, Parkinson's disease, and stroke.[4]
       Recently, TUDCA has been found to have protective effects in the
       eye, especially concerning retinal degenerative disorders.
       Contents  [hide]
       1
       History
       2
       Cellular mechanism
       3
       Current research
       3.1
       Photoreceptor cells
       3.2
       Choroidal neovascularization
       3.3
       Synaptic connectivity
       4
       See also
       5
       References
       History[edit]
       Chinese medicine has used animal bile for hundreds of years as a
       medicine to treat "heat" illnesses. It was used to relieve
       spasms, reduce fever, and improve visual acuity. Bile is
       naturally synthesized via cholesterol, consisting of compounds
       including taurochenodeoxycholic acid, ursodeoxycholic acid, and
       chenodeoxycholic acid.[5] However, UDCA and TUDCA were first
       synthetically developed in 1954 in Japan.[4]
       Cellular mechanism[edit]
       Apoptosis, or programmed cell death, is largely influenced by
       the mitochondria. If the mitochondria are distressed, they
       release the molecule cytochrome C (cyC). Cytochrome C initiates
       enzymes called caspases to propagate a cascade of cellular
       mechanisms to cause apoptosis. TUDCA prevents apoptosis with its
       role in the Bax pathway. Bax, a molecule that is translocated to
       the mitochondria to release cytochrome C, initiates the cellular
       pathway of apoptosis.[4] TUDCA prevents Bax from being
       transported to the mitochondria. This protects the mitochondria
       from perturbation and the activation of caspases.[6] TUDCA acts
       as a chemical chaperone.
       Current research[edit]
       Studies in recent years are continually showing ocular
       protective effects via TUDCA.
       Photoreceptor cells[edit]
       A study examined the effects of TUDCA on cones, in relation to
       retinitis pigmentosa (RP), a disease in which retinal rods and
       cones undergo apoptosis. Mice models were used, a wild-type and
       a mutant RP model, rd10. Both models were injected with TUDCA
       every 3 days from post-natal day 6 (p6) to p30 and compared to
       the vehicle. Electroretinography (ERG), photoreceptor cell
       counts, cone photoreceptor nuclei counts, and TUNEL labeling
       were all analyzed to show the effects of TUDCA. The dark-adapted
       and light-adapted ERG responses were greater in the TUDCA
       treated mouse than the vehicle treated mouse. TUDCA treated mice
       also had more photoreceptor counts, yet non-altered retinal
       morphology or function. Even at P30, a stage where rod and cone
       function is usually greatly diminished in the rd10 mouse model,
       the photoreceptor function was protected.[7]
       Another study, from the Department of Ophthalmology at Johns
       Hopkins University, in Baltimore, Maryland, saw similar effects
       in two components of bile, bilirubin and TUDCA, in relation to
       RP. Oxidative stress and prolonged light exposure were studied
       in rd10 mice and albino mice. In rd10 mice, intraperitoneal
       injections of bilirubin or TUDCA were given every 3 days
       starting at P6. This caused a considerable preservation in cone
       cell amount and function at P50, and a modest rod cell amount at
       P30. In the albino mice models, intraperitoneal injections of
       bilirubin or TUDCA were given prior to prolonged light exposure.
       Both treatments had positive effects on the health of the mouse
       retina, including a reduced accumulation of superoxide radicals,
       rod cell death, and disruption of cone inner and outer segments.
       The findings of the study are elucidating optimized conditions
       for RP treatment[8]
       Choroidal neovascularization[edit]
       A study done at the Department of Ophthalmology at Seoul
       National University College of Medicine, examined the effects of
       TUDCA and UDCA on laser-treated choroids of rat models. Argon
       lasers were used to induce choroidal neovascularization (CNV) in
       rat models. TUDCA and UDCA were injected intraperitoneally 24
       hours before and daily after the laser treatment. Fourteen days
       after laser-treatment, the eyes were examined for effects.
       Fluorescein angiography showed lower leakage from the CNV in
       UDCA and TUDCA treated groups than the control group.
       Additionally, vascular endothelial growth factor (VEGF) levels
       in the retina were examined and showed lower levels in the TUDCA
       treated group compared to the control group, whereas no effect
       in the UDCA treated group. TUDCA and UDCA may suppress CNV
       formation, which may be associated with its anti-inflammatory
       effects.[9]
       Synaptic connectivity[edit]
       A study from the Department of Physiology in University of
       Alicante, in Alicante, Spain, shows the effects of TUDCA in the
       P23H transgenic rat, a model of autosomal dominant retinitis
       pigmentosa. The transgenic rats were injected with TUDCA once a
       week starting from P21 until P120, along with
       vehicle-administered controls. At P120, the functionality of the
       retina was examined via ERG and immunoflourescent microscopy.
       The amplitude of the a- and b- waves were considerably higher in
       TUDCA treated rats, compared to the control group. Photoreceptor
       density in the center of the retina was three-fold greater in
       TUDCA treated rats. Also, TUNEL results showed smaller amounts
       of TUNEL-positive cells. The synaptic contacts amongst
       photoreceptor cells, bipolar cells, and horizontal cells were
       preserved in the TUDCA treated P23H rats. Additionally, the
       synaptic terminals in the outer plexiform layer were of greater
       density that in control rats. The neuroprotective effects of
       TUDCA are not only preserving retinal morphology and function,
       but also its synaptic contacts, a potentially useful aspect in
       delaying RP.[10]
       See also[edit]
       Taurolithocholic acid
       Taurochenodeoxycholic acid, an epimer
       References[edit]
       Jump up
       ^ Boatright, Jeffrey H.; Nickerson, John M.; Moring, Anisha G.;
       Pardue, Machelle T. (2009). "Bile acids in treatment of ocular
       disease". Journal of Ocular Biology, Diseases, and Informatics.
       2 (3): 149–159. doi:10.1007/s12177-009-9030-x. PMC
       2798994 . PMID 20046852.
       Jump up
       ^ Boatright JH, Nickerson JM, Moring AG, Pardue MT (2009). "Bile
       acids in treatment of ocular disease". J Ocul Biol Dis Infor. 2
       (3): 149–159. doi:10.1007/s12177-009-9030-x. PMC 2798994 .
       PMID 20046852.
       Jump up
       ^ Duan, WJ, Zhang, FK, Ou XJ, Zhang, T, Wang, XM, Wang, Y, Cui,
       Y, Zhao, XY, Jia, JD (2011). "[The clinical profiles of primary
       biliary cirrhosis with a suf the best sup around for saving the
       liver from alcohol or oral cycles.
       #Post#: 856--------------------------------------------------
       Re: TUDCA
       By: Rot-Iron66 Date: June 27, 2022, 3:39 am
       ---------------------------------------------------------
       Ive always used the capsules.
       I just got the powder (Nutricost) and have been adding it to my
       Intra, but good-lord is this stuff awful tasting.
       Ill be going back to the capsules when this is used up.
       Ruins the whole tase of any drink.  :(
       #Post#: 858--------------------------------------------------
       Re: TUDCA
       By: Road2HardCoreIron Date: June 27, 2022, 4:19 am
       ---------------------------------------------------------
       Yes bad enough you taste it on the capsules. I can't think
       without.  It lingers in your mouth for awhile.
       #Post#: 1562--------------------------------------------------
       Re: TUDCA
       By: Max Plateman Date: November 16, 2022, 8:44 pm
       ---------------------------------------------------------
       What doses are you guys taking and when?
       #Post#: 1573--------------------------------------------------
       Re: TUDCA
       By: Road2HardCoreIron Date: November 17, 2022, 11:51 am
       ---------------------------------------------------------
       I use 250 x2 a day.  This time.  I' going to follow up with my 3
       month TRT labs
       #Post#: 1574--------------------------------------------------
       Re: TUDCA
       By: Road2HardCoreIron Date: November 17, 2022, 11:52 am
       ---------------------------------------------------------
       I'm using UDCA THE PHARMA brand.
       [quote author=Big Chicken link=topic=171.msg1573#msg1573
       date=1668707496]
       I use 250 x2 a day.  This time.  I' going to follow up with my 3
       month TRT labs
       [/quote]
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