Protective effects of recombinant human growth hormone on cirrhotic rats

Chen, Shuang; Wang, Hong-Tao; Yang, Bin; Fu, Yu-ru; Ou, Qing-Jia

doi:10.3748/wjg.v10.i19.2894

Cited by 8 publications

(5 citation statements)

References 41 publications

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“…Administration of GH in addition to MTX reduced the effects of MTX on sperm parameters and testosterone concentration completely or partially. The role of GH in protecting and regenerating testicular tissue after chemotherapy with cyclophosphamide (Satoh et al, 2002), improving liver function, increasing albumine and superoxide dismutase, decreasing serum alanine transaminase and collagen rates and healing liver cirrhosis in rats have already been studied (Chen et al, 2004). This study showed that there were no significant differences in testicular and body weight, number, motility and viability of spermatozoa and testosterone concentration between GH and control group.…”

Section: Discussionmentioning

confidence: 71%

Effect of growth hormone on testicular dysfunction induced by methotrexate in rats

Nouri

Azarmi²,

Movahedin

2009

Andrologia

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Methotrexate (MTX) is a chemotherapeutic agent causing defective oogenesis and spermatogenesis. This study was performed to assess the role of human growth hormone (GH) on testis recovery after treatment with MTX. Forty male Wistar rats were selected and randomly divided into four groups (n = 10): control (vehicle), GH group (0.3 mg kg(-1) GH for 28 days, IP), MTX group (MTX 1 mg kg(-1) week(-1) for 4 weeks, IP) and GH/MTX group (0.3 mg kg(-1) GH for 28 day plus 1 mg kg(-1) week(-1) MTX for 4 weeks, IP). On days 14 and 28, five rats from each group were killed, testes of rats of all groups were removed, spermatozoa were collected from epididymis and then prepared for analysis. MTX caused significant increase in interstitial tissue and capsular thickness and decrease of testicular and body weight (P < 0.05). Moreover, it caused significant decline in seminiferous tubule diameter and epithelium thickness (P < 0.05). There was no obvious change in morphometrical parameters between MTX/GH and control groups. In MTX group, sperm parameters decreased significantly (P < 0.05). Administration of GH plus MTX reduced the effects of MTX on sperm parameters and testosterone concentration. These results suggested that GH had a protective effect on almost all destructive effects caused by MTX in rat testes and thus improved sperm parameters.

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Section: Discussionmentioning

confidence: 71%

Effect of growth hormone on testicular dysfunction induced by methotrexate in rats

Nouri

Azarmi²,

Movahedin

2009

Andrologia

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“…[ 31 ] TAA is metabolized in the liver by flavin containing monozygenase (mixed function oxidase system) and finally becomes TAA-S-oxide metabolite (TASO). [ 32 ] TASO is subsequently transformed into TAA S, S-dioxide with or without being further oxidized to form species that exert their toxic effect on several organs, including plasma, liver, kidney, bone marrow, adrenals, and other tissues. TAA undergoes an extensive metabolism to acetate, and it is finally excreted through the urine within 24 h.[ 33 ] It was described that the mechanism of TAA hepatotoxicity may be that TAA acts as creator of ROS leading to lipid peroxidation, oxidation of cellular proteins and extensive mitochondrial DNA strand breakage, thus inducing impairment of mitochondrial protein synthesis.…”

Section: Resultsmentioning

confidence: 99%

Protective effect of calycosin-7-O-β-D-glucopyranoside against oxidative stress of BRL-3A cells induced by thioacetamide

Li¹,

Lin²,

Ma³

et al. 2015

Phcog Mag

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Background:Calycosin-7-O-β-D-glucopyranoside (CG) is a natural isoflavone found in traditional Chinese medicines Astragali Radix (AR).Objective:Calycosin-7-O-β-D-glucopyranoside, an isoflavone isolated from AR, has been found to have potent antioxidantive effects. This study was designed to investigate whether CG prevents oxidative stress induced by thioacetamide (TAA).Materials and Methods:BRL-3A cells were pretreated with different concentrations of CG (10, 20, 40 mg/mL) for 12 h and then exposed to 0.18 mol/L TAA for 2 h. The cell viability were examined by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium assay, total antioxidant capacity, malondialdehyde (MDA) and the activity of antioxidant enzymes, including catalase, glutathione peroxidase and superoxide dismutase were determined by microplate method. Reactive oxygen species (ROS) generation was quantified by the 2’,7’-dichlorofluorescin-diacetate method. Protein and mRNA expression of CYP2E1 were determined by western blotting and real-time PCR.Results:The cell oxidative stress was significantly increased after 2 h of TAA exposure. Pretreatment of BRL-3A cells with CG significantly increased the activities of antioxidant enzymes, scavenged ROS and reduced MDA production. CG decreased the expression of CYP2E1, and ultimately decreased TAA-induced BRL-3A cells oxidative stress.Conclusions:Calycosin-7-O-β-D-glucopyranoside has a protective effect against TAA-induced oxidative stress in BRL-3A cells, and that the underlying mechanism involves in scavenging of ROS and the modulating expression of CYP2E1.

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“…In turn, the oral administration of TAA would provide the new experimental model (group 4) with both liver cirrhosis 11,19,27 and an increase in PP 11,28 (Fig. 1).…”

Section: Mean±sdmentioning

confidence: 98%

Partial Portal Vein Ligation Plus Thioacetamide: A Method to Obtain a New Model of Cirrhosis and Chronic Portal Hypertension in the Rat

Méndez-López

Méndez

Sánchez-Patán

et al. 2007

Journal of Gastrointestinal Surgery

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To obtain a new model of chronic portal hypertension in the rat, two classical methods to produce portal hypertension, partial portal vein ligation and the oral administration of thioacetamide (TAA), have been combined. Male Wistar rats were divided into four groups: 1 (control; n = 10), 2 [triple partial portal vein ligation (TPVL); n = 9], 3 (TAA; n = 11), and 4 (TPVL plus TAA; n = 9). After 3 months, portal pressure, types of portosystemic collateral circulation, laboratory hepatic function tests (aspartate aminotransferase, alanine aminotransferase, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase) and liver histology were studied. The animals belonging to group 2 (TPVL) developed extrahepatic portosystemic collateral circulation, associated with mesenteric venous vasculopathy without hepatic destructurization or portal hypertension. Animals from group 3 (TAA) developed cirrhosis and portal hypertension but not extrahepatic portosystemic collateral circulation, or mesenteric venous vasculopathy. Finally, the animals from group 4 (TPVL + TAA) developed cirrhosis, portal hypertension, portosystemic collateral circulation, and mesenteric venous vasculopathy. The association of TPVL and TAA can be used to obtain a model of chronic portal hypertension in the rat that includes all the alterations that patients with hepatic cirrhosis usually have. This could, therefore, prove to be a useful tool to study the pathophysiological mechanisms involved in these alterations.

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Protective effects of recombinant human growth hormone on cirrhotic rats

Cited by 8 publications

References 41 publications

Effect of growth hormone on testicular dysfunction induced by methotrexate in rats

Effect of growth hormone on testicular dysfunction induced by methotrexate in rats

Protective effect of calycosin-7-O-β-D-glucopyranoside against oxidative stress of BRL-3A cells induced by thioacetamide

Partial Portal Vein Ligation Plus Thioacetamide: A Method to Obtain a New Model of Cirrhosis and Chronic Portal Hypertension in the Rat

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