Ten Scientific Studies Mentioning Alpha Lipoic Acid -- Out Of 1231 Total
[Karl
Note: Obviously Alpha Lipoic Acid is a popular
substance -- with more than 1000 separate scientific
references to this substance. The ten top items are
shown below, and then a few selected abstracts further
below. The first four references are actually
published at the bottom of the page -- click on the link
to jump to them. The remaining references have web
addresses you can use to go to that abstract.]
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Protective effect of alpha-lipoic acid
against ischaemic acute renal failure in rats.
Takaoka M, Ohkita M, Kobayashi Y, Yuba M, Matsumura Y.
Department of Pharmacology, Osaka University of
Pharmaceutical Sciences, Osaka, Japan.
1. In the present study, we investigated whether
treatment with alpha-lipoic acid (LA), a powerful and
universal anti-oxidant, has renal protective effects in
rats with ischaemic acute renal failure (ARF). 2.
Ischaemic ARF was induced by occlusion of the left renal
artery and vein for 45 min followed by reperfusion, 2
weeks after contralateral nephrectomy. Blood urea
nitrogen (BUN), plasma concentrations of creatinine (Pcr)
and urinary osmolality (Uosm) were measured for the
assessment of renal dysfunction. Creatinine clearance (Ccr)
and fractional excretion of Na+ (FENa) were used as
indicators of glomerular and tubular function,
respectively. 3. Renal function in ARF rats decreased
markedly 24 h after reperfusion. Intraperitoneal
injection of LA at a dose of 10 mg/kg before the
occlusion tended to attenuate the deterioration of renal
function. A higher dose of LA (100 mg/kg) significantly
(P < 0.01) attenuated the ischaemia/reperfusion-induced
increases in BUN (19.1 +/- 0.7 vs 7.2 +/- 0.7 mmol/L
before and after treatment, respectively), Pcr (290 +/-
36 vs 78.1 +/- 4.2 micromol/L before and after treatment,
respectively) and FENa (1.39 +/- 0.3 vs 0.33 +/- 0.09%
before and after treatment, respectively). Treatment with
100 mg/kg LA significantly (P < 0.01) increased Ccr (0.70
+/- 0.13 vs 2.98 +/- 0.27 mL/min per kg before and after
treatment, respectively) and Uosm (474 +/- 39 vs 1096 +/-
80 mOsmol/kg before and after treatment, respectively).
4. Histopathological examination of the kidney of ARF
rats revealed severe lesions. Tubular necrosis (P <
0.01), proteinaceous casts in tubuli (P < 0.01) and
medullary congestion (P < 0.05) were significantly
suppressed by the higher dose of LA. 5. A marked increase
in endothelin (ET)-1 content in the kidney after
ischaemia/reperfusion was evident in ARF rats (0.43 +/-
0.02 ng/g tissue) compared with findings in sham-
operated rats (0.20 +/- 0.01 ng/g tissue). Significant
attenuation (P < 0.01) of this increase occurred in ARF
rats treated with the higher dose of LA (0.24 +/- 0.03 ng/g
tissue). 6. These results suggest that administration of
LA to rats prior to development of ischaemic ARF prevents
renal dysfunction and tissue injury, possibly through the
suppression of overproduction of ET-1 in the
postischaemic kidney.
PMID: 11906481 [PubMed - in process]
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Elimination of *O2minus sign/H2O2 by
alpha-lipoic acid mediates the recovery of basal EDRF/NO
availability and the reversal of superoxide dismutase-induced
relaxation in diabetic rat aorta.
Kocak G, Karasu C.
Department of Pharmacology, Faculty of Pharmacy, Ankara
University, Ankara, Turkey.
AIM: The aims of this study were to ascertain the
mechanism(s) of relaxant action of exogenous superoxide
dismutase (SOD) in aortic rings obtained from 12-week,
streptozotocin(STZ)-diabetic and age-matched control
rats, and to examine the effects of alpha-lipoic acid
(ALA) treatment (for 6 weeks, after 6 weeks of untreated
diabetes) on SOD-induced relaxations. MATERIALS AND
METHODS: Thoracic aorta rings were suspended to isolated
tissue chamber, and the changes in isometric tension were
recorded. RESULTS: SOD produced a greater relaxation in
untreated-diabetic rings compared with control rings. ALA
treatment partially reversed SOD-induced relaxation in
diabetic aorta. Pretreatment of rings with NG-nitro-l-arginine
methyl ester (L-NAME, 100 microm) inhibited SOD-induced
relaxation. This effect of L-NAME was markedly observed
in control and ALA-treated-diabetic rings compared with
untreated-diabetic rings. SOD-induced relaxation was also
inhibited by catalase (60 U/ml) in untreated-diabetic
rings but not in ALA-treated-diabetic and control rings.
Pretreatment with the cyclooxygenase inhibitor,
indomethacin, or the catalase inhibitor, aminotriazole,
had no effect on SOD-induced relaxation in any ring.
CONCLUSION: Findings suggested that: (i) in normal
physiological conditions, the relaxant effect of SOD is
related to the inhibition of superoxide anion radicals
(*O2minus sign)-induced endothelium-derived relaxing
factor/nitric oxide (EDRF/NO) destruction in the rat
aorta; (ii) in diabetic state, excess *O2minus sign
increasingly inhibits basal EDRF/NO, and the dismutation
of excess *O2minus sign to H2O2 is enhanced by exogenous
SOD. H2O2 a vasorelaxant molecule, which probably
accounts for the increased responsiveness of diabetic
rings to exogenous SOD; and (iii) the reversal effect of
in vivo ALA treatment on SOD-induced relaxation in
diabetic aorta is probably linked with the elimination of
*O2minus sign/H2O2, which mediates the recovery of basal
EDRF/NO availability.
PMID: 11874445 [PubMed - in process]
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Lipoic acid increases glucose uptake
by skeletal muscles of obese-diabetic ob/ob mice.
Eason RC, Archer HE, Akhtar S, Bailey CJ.
School of Pharmacy, Aston University, Birmingham, UK.
AIM: Alpha-lipoic acid has been reported to increase
glucose disposal in diabetic states. This study has
examined the effect of alpha-lipoic acid on glucose
uptake by cultured L6 muscle cells and different types of
skeletal muscles in normal lean (+/+) and severely
insulin-resistant, obese-diabetic (ob/ob) mice. METHODS:
Glucose uptake was measured in L6 muscle cells using the
non-metabolized glucose analogue 2-deoxy-d-glucose (2DG),
and in isolated muscles by glucose disappearance from the
incubation medium. RESULTS: In L6 muscle cells,
short-term incubations (2-12 h) with 10(-3) m alpha-lipoic
acid increased glucose uptake by 40-80%, approximately
the same extent as 10(-6) m insulin. Combination of the
two agents produced a slightly greater increase (120% at
12 h) than either alone. Red quadriceps (mainly type 1
fibres), diaphragm (similar proportions of type 1 and 2
fibres) and abdominal muscle (mainly type 2 fibres) from
normal mice incubated with 10(-3) m alpha-lipoic acid
showed increased glucose uptake to a similar extent as
10(-6) m insulin in each of the three muscles. Muscles
from ob/ob mice, which showed little response to insulin,
showed a substantial increase (approximately 300%, p <
0.05-0.01) in glucose uptake when 10(-3) m alpha-lipoic
acid was added in the presence of insulin. The alpha-lipoic
acid also increased glucose uptake in red quadriceps
(approximately 300%, p < 0.01) from ob/ob mice without
added insulin. CONCLUSION: The results suggest that
alpha-lipoic acid can increase glucose uptake by a range
of normal muscle types and improve the response to
insulin by insulin-resistant skeletal muscles of ob/ob
mice.
PMID: 11874439 [PubMed - in process]
Beneficial effects of alpha-lipoic
acid plus vitamin E on neurological deficit, reactive
gliosis and neuronal remodeling in the penumbra of the
ischemic rat brain.
Gonzalez-Perez O, Gonzalez-Castaneda RE, Huerta M,
Luquin S, Gomez-Pinedo U, Sanchez-Almaraz E, Navarro-Ruiz
A, Garcia-Estrada J.
Division de Neurociencias, Centro de Investigacion
Biomedica de Occidente (CIBO) del Instituto Mexicano del
Seguro Social (IMSS), Sierra Mojada 800, 44340,
Guadalajara Jalisco, Mexico
During cerebral ischemia-reperfusion, the enhanced
production of oxygen-derived free radicals contributes to
neuronal death. The antioxidants alpha-lipoic acid and
vitamin E have shown synergistic effects against lipid
peroxidation by oxidant radicals in several pathological
conditions. A thromboembolic stroke model in rats was
used to analyze the effects of this mixture under two
oral treatments: intensive and prophylactic. Neurological
functions, glial reactivity and neuronal remodeling were
assessed after experimental infarction. Neurological
recovery was only found in the prophylactic group, and
both antioxidant schemes produced down-regulation of
astrocytic and microglial reactivity, as well as higher
neuronal remodeling in the penumbra area, as compared
with controls. The beneficial effects of this antioxidant
mixture suggest that it may be valuable for the treatment
of cerebral ischemia in humans.
PMID: 11872266 [PubMed - in process]
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