The Effects of Dimethylsulfoxide in Experimental Obstructive Jaundice

Küçük, Can; Ok, Engin; Yılmaz, Zeki; Sözüer, Erdoğan; Muhtaroğlu, Sabahattin; Arar, Makbule

doi:10.1080/00015458.2003.11679450

Cited by 10 publications

(8 citation statements)

References 17 publications

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“…MDA is an end product of lipid peroxidation and is a good indicator of oxidative stress. Consistent with previously reported findings from studies of obstructive jaundice in rodents [12,[18][19][20], BDL in RLS-treated rats was associated with increased hepatic levels of MDA. There are also several endogenous antioxidant enzymes, for example, superoxide dismutase, catalase, and glutathione peroxidase that maintain an imbalance between ROS and the anti-oxidative defense system.…”

Section: Discussionsupporting

confidence: 91%

Ethyl Pyruvate Prevents Intestinal Inflammatory Response and Oxidative Stress in a Rat Model of Extrahepatic Cholestasis

Wang

Gong

Wei

et al. 2010

Journal of Surgical Research

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Section: Discussionsupporting

confidence: 91%

Ethyl Pyruvate Prevents Intestinal Inflammatory Response and Oxidative Stress in a Rat Model of Extrahepatic Cholestasis

Wang

Gong

Wei

et al. 2010

Journal of Surgical Research

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“…Consistent with previously reported findings from studies of obstructive jaundice in rodents (15)(16)(17)(18), CBDL in RLS-treated mice was associated with increased hepatic levels of MDA, a marker of lipid peroxidation and redox stress. When the mice with obstructive jaundice were treated with REPS, hepatic MDA levels were normalized.…”

Section: Discussionsupporting

confidence: 91%

“…The total RNA was treated with DNAFree (Ambion, Houston, TX) as instructed by the manufacturer using 10 units of DNase I/10 g RNA. Two micrograms of total RNA was reverse transcribed in a 40-L reaction volume containing 0.5 g of oligo(dT) 15 (Promega), 1 mM of each dNTP, 15 U AMV reverse transcriptase (Promega), and 1 U/L of recombinant RNasin ribonuclease inhibitor (Promega) in 5 mM MgCl 2 , 10 mM Tris-HCl, 50 mM KCL, 0.1% Triton X-100 (pH 8.0). The reaction mixtures were preincubated at 21°C for 10 min before DNA synthesis.…”

Section: Reverse Transcriptase Polymerase Chain Reaction (Rt-pcr)mentioning

confidence: 99%

Ethyl Pyruvate Reduces Liver Injury in a Murine Model of Extrahepatic Cholestasis

Yang¹,

Uchiyama²,

Watkins³

et al. 2004

Shock

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Ethyl pyruvate has been shown to ameliorate liver injury and decrease expression of several proinflammatory cytokines when used to treat mice with hemorrhagic shock or alcoholic hepatitis. Herein we sought to determine whether delayed treatment with ethyl pyruvate dissolved in a Ringer's-type balanced salt solution--Ringer's ethyl pyruvate solution (REPS)--would be beneficial in a murine model of common bile duct ligation (CBDL)-induced liver injury. Male C57BL/6 mice were subjected to a sham (n = 6) procedure or CBDL (n = 27). Twenty-four hours after operation, mice subjected to CBDL were randomized to receive treatment with either REPS (40 mg/kg of ethyl pyruvate per dose) or Ringer's lactate solution (RLS) every 8 h over a 72 h period. Compared with sham-treated controls, CBDL in RLS-treated mice was associated with histological evidence of hepatocellular necrosis as well as significant increases in the plasma concentrations of alanine aminotransferase and total bilirubin. Relative to sham-treated controls, CBDL in RLS-treated mice also was associated with increased hepatic lipid peroxidation and increased hepatic expression of transcripts for TNF, IL-6, and iNOS. All of these changes were significantly attenuated by delayed treatment with REPS after CBDL. In the RLS-treated group, CBDL was associated with increased NF-kappaB DNA binding in nuclear extracts prepared from liver tissue. Treatment with REPS increased NF-kappaB DNA binding still further. CBDL was associated with increased hepatocellular apoptosis in both the RLS- and REPS-treated groups. These data support the view that ethyl pyruvate ameliorates hepatic inflammation, lipid peroxidation, and necrosis in mice subjected to CBDL. Ethyl pyruvate warrants further evaluation as an adjunctive treatment to ameliorate liver injury from extrahepatic biliary obstruction.

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“…Ultrastructural findings in the present study were similar to those reported after inflammation-derived demyelinating diseases of the peripheral nervous system. Increased levels of free oxygen radicals (FOR), TNF, ILs, NO and several other cytokines have been reported in both inflammatory demyelinating neuropathies and OJ [17][18][19]. In the current study, levels of above-mentioned cytokines were not measured again because these were shown to rise rapidly in the experimental and/or clinical OJ previously [7,8,[19][20][21][22][23].…”

Section: Discussionmentioning

confidence: 94%

Effects of Obstructive Jaundice on the Peripheral Nerve: An Ultrastructural Study in Rats

Can

Saray²,

Caglikulekci³

et al. 2004

Eur Surg Res

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Obstructive jaundice (OJ) and hepatic disorders have been shown to be associated with peripheral neuropathy in several clinical studies. The study evaluated the effect of OJ on the ultrastructure of the rat sciatic nerve. In the OJ group, jaundice was created by ligation of common bile duct in Wistar-Albino rats. In the sham-operated control group the same procedure was performed without ligation of the bile duct. On day 7, all rats were re-operated and sciatic nerves were explored to harvest 2-cm-long nerve segments for quantitative and qualitative histopathological analysis by light and electron microscopy. Bilirubin was measured on serum samples. Bilirubin levels were significantly higher in jaundiced rats compared with that of controls (8.46 ± 0.45 vs. 0.80 ± 0.14 mmol/l, means ± SD, p < 0.01). Control nerves did not show anything other than the normal histology. In the OJ group, degenerative changes such as irregularities, thinning, ruffling and invaginations, irregularshaped bodies, vacuolizations and focal segmental demyelination were observed in the myelin sheath. Myelin clusters were noted in the axoplasm. A varying degree of swelling was noted in the nucleus and cytoplasm of the Schwann cells. Morphometric analysis of specimens obtained from sciatic nerves showed that myelin injury (370.9 ± 51.3 vs. 11.6 ± 0.5 axons), axonal edema (142.1 ± 24.2 vs. 10.6 ± 0.5 edematous axons) and Schwann cell degeneration (50.3 ± 11.6 vs. 3.2 ± 0.2 Schwann cells) was significantly higher in the jaundiced rats than in the control group (p < 0.01). The ultrastructural alterations spotted in the rat peripheral nerve were attributed to hyperbilirubinemia and increased concentrations of several neurotoxic substances released from the Kupffer cells in OJ. Neuropathy in jaundiced patients seems to result from accompanying degenerative changes in the peripheral nervous system. However, the exact nature and initiating factors of this nerve injury remains to be unveiled.

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The Effects of Dimethylsulfoxide in Experimental Obstructive Jaundice

Cited by 10 publications

References 17 publications

Ethyl Pyruvate Prevents Intestinal Inflammatory Response and Oxidative Stress in a Rat Model of Extrahepatic Cholestasis

Ethyl Pyruvate Prevents Intestinal Inflammatory Response and Oxidative Stress in a Rat Model of Extrahepatic Cholestasis

Ethyl Pyruvate Reduces Liver Injury in a Murine Model of Extrahepatic Cholestasis

Effects of Obstructive Jaundice on the Peripheral Nerve: An Ultrastructural Study in Rats

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