Hepato-renal and hematological effects of flunixin and silymarin coadministration in rats

Mohammed, Imtithal A.; Shaban, Khalid A.; Albadrany, Yasser M.

doi:10.33899/ijvs.2021.130323.1800

Cited by 7 publications

(7 citation statements)

References 20 publications

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“…The results of our current study presented a significant enhancement in the activities of the liver enzymes AST, ALT and ALK as well as the levels of total bilirubin in the blood serum after administering silymarin to animals compared with the group of animals treated with TAA. Treating rabbits with TAA caused an increase in the activity of AST, ALT and ALK enzymes, while no increase was observed in animals treated with silymarin, indicating the protective activity of silymarin against TAA (31,32).While Ghosh (33) and Kim (34) showed (33,34) showed that administration of silymarin to mice treated with TAA for a time of 56 days caused a decrease in the activity of ALT, AST and ALK, besides an increase in the activity of anti-oxidant enzymes SOD, MDA and CAT, indicating the effectiveness of silymarin as an antioxidant and a hepatoprotective against the effect of TAA (35,36). Through its role in reducing the programmed death of hepatocytes and stimulating the PI3K-Akt cell survival pathway (37)(38)(39).…”

Section: Discussionmentioning

confidence: 94%

Development of an experimental hepatic encephalopathy in a rabbit model: Biochemical and immunohistochemical study

Faisul¹,

Al-Saidya²

2022

IJVS

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This study was designed to estimate the biochemical, histochemical, and immunohistochemical aspects of hepatic encephalopathy (HE) induced experimentally by using Thioacetamide (TAA). Twenty-four male rabbits were separated into four main groups (6 each), the Control group (group I) and Group II; rabbits were injected with TAA dissolved in distal water at 200 mg/kg B.W. twice weekly for eight weeks. Group III was given silymarin orally dissolved in saline 200mg/kg B.W. daily for eight weeks. Group IV animals received TAA and Silymarin 200 mg/kg B.W. for eight weeks. The results revealed animals treated with TAA indicated a significant decrease in the level of TSP and a significant increase in the levels of TSB, ALP, ALT, and AST. Histopathological examination of each liver and brain indicates necrosis of the hepatocytes, Cholangitis, biliary duct epithelium hyperplasia and preductular fibrosis, and collagen fiber deposition in the portal triad. Necrosis of the neurons, Purkinjean, and molecular cells with a decrease in granular cells and thickening of meninges. The histochemical examination of the liver revealed the presence of fibrosis in the portal area and the peri-lobular septa and the presence portal to portal bridging fibrosis. The immunohistochemical stain of the liver section revealed a positive reaction for collagen type IV, especially in/and around the portal tried as well as in the septa between the lobules. In conclusion, in rabbit's model, hepatotoxicity to the early stages of the pathogenesis of hepatoencephalopathy.

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Section: Discussionmentioning

confidence: 94%

Development of an experimental hepatic encephalopathy in a rabbit model: Biochemical and immunohistochemical study

Faisul¹,

Al-Saidya²

2022

IJVS

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“…As we know hydrazine derivatives cause protein denaturation and saponifying adipose tissue, the results indicate that rats' livers treated with DMH in a dose of 10 and 20 mg/kg bw reveals vacuolar degeneration, necrosis, hemorrhage and infiltration of inflammatory cells this lesion occurs due to a toxic free-radical that produced by the dimethylhydrazine administration this indicated by increased serum level of AST and ALT which cause liver injury (25)(26)(27). DMH consider a stronger hepatic and colonic carcinogen cause hepatic tissue injury, oxidative stress and mutation of DNA which metabolized in liver to carbonium ion and oxy radicals that leads to Wnt signaling pathway activation this in turn cause increased proliferation and inflammation of hepatocyte that indicated by increased level of cyclooxygenase 2 enzyme (COX-2) (8).…”

Section: Discussionmentioning

confidence: 99%

Histopathological evaluation of lesions induced by dimethyl hydrazine in male rats

Al-Hamdany¹,

Al-Mallah²,

Ismail³

2022

IJVS

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This study evaluated dimethylhydrazines' carcinogenic and toxic effect (DMH) in male rats; 30 albino rats were divided into three groups, randomly ten rates for each one. Group 1 control group was lifted for water only, group 2 was treated with DMH at a dose of 10 mg /kg bw in 0.9% sodium chloride subcutaneously once weekly for eight weeks, and group 3 was treated with DMH at a dose of 20 mg /kg bw in 0.9% NaCl subcutaneously once weekly for eight weeks. Liver grossly congested with pinpoint hemorrhage in a dose of 10 mg/kg of bw and enlarged in a dose of 20 mg/kg bw. Congestion of blood vessels in the heart with hypertrophy of myocardium in a dose of 20 mg/kg bw. Kidney grossly appears normal in both doses. Lesions of the liver treated with DMH in the dose 10 mg/kg BW show discontinuation of hepatocytes, infiltrations of inflammatory cells, and vacuolar degeneration of hepatocytes with apoptotic bodies. Section of the liver treated with DMH in the dose 20 mg/kg BW shows acute hemorrhage and focal necrosis of hepatocytes with edema. Heart treated with DMH in a dose of 10 mg/kg BW shows discontinuation of myocardial muscle fibers and infiltrations of inflammatory cells. In contrast, lesions in the dose 20 mg/kg bw show foci of inflammatory cells with cardiomyopathies of myocardium and congestion of blood vessels. Kidney treated with DMH in a dose of 10 mg/kg BW shows degeneration of epithelial cells lining renal tubule, infiltrations of inflammatory cells, hyaline cast with atrophy of glomerular tuft, increased space of Bauman's, and cloudy swelling. The kidney section treated with DMH in a dose of 20 mg/kg bw shows hemorrhage between renal tubules, congestion of blood vessels, infiltrations of inflammatory cells, a renal cyst, and degeneration of glomeruli.

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“…In our study, we determined that silymarin ameliorated the histopathological changes in the glomerulus and tubular epithelium caused by Tacrolimus. In experimental animal drug nephrotoxicity studies, it was determined that silymarin was protective against renal toxicity by lowering the serum creatinine level [ 13 , 43 , 59 , 60 ]. In this study, the creatinine level was significantly decreased in the Tac + SLI 200 group compared to the Tac group ( P < 0.05).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of silymarin on tacrolimus-induced kidney and liver toxicity

Terzi

Çiftçi

2022

BMC Complement Med Ther

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Background Tacrolimus (FK506) is an immunosuppressive agent and has toxic side effects such as nephrotoxicity, hepatotoxicity, and neurotoxicity. In our study, we aimed to investigate the protective effect of silymarin on renal and hepatic toxicity considered to be tacrolimus related. Methods In this 6-week experimental study, 46 eight-week-old healthy male rats were used. The groups comprised the Control (healthy rats, n = 6), Tac (tacrolimus 1 mg/kg, n = 8), silymarin 100 mg/kg (SLI 100 mg/kg n = 8), Tac + SLI 100 (tacrolimus 1 mg/kg + SLI 100 n = 8), SLI 200 (SLI 200 mg/kg n = 8), and Tac + SLI 200 (tacrolimus 1 mg/kg + SLI 200 mg/kg n = 8). After 6 weeks, all rats were sacrificed, and the tissue follow-up procedure was performed for kidney and liver tissues, histopathology, and in situ TUNEL analysis. Blood samples were analyzed for the total antioxidant capacity (TAC), total oxidant capacity (TOC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), albumin, total bilirubin, creatine. Results Histopathological findings of kidney and liver tissue of rats were determined to increase statistically in Tac group compared to SLI 1 00 and SLI 200 groups (P < 0.05). In addition, the Tac + SLI 100 and Tac + SLI 200 groups were found to be statistically similar to the Control group (P > 0.05). The in situ TUNEL method showed that the tacrolimus increased apoptosis while the silymarin decreased it. TOC levels increased statistically in Tac groups compared to silymarin-treated groups (P < 0.05). Although the TAC level was not statistically significant among the experimental groups (P > 0.05), the lowest was measured in the Tac group. The ALT, AST, GGT, total bilirubin, and creatine values were higher in the Tac group than in the silymarin groups (P < 0.05). There was no statistically significant difference between the groups with regard to the albumin level (P > 0.05). Conclusion In our study, we determined that tacrolimus caused damage to kidney and liver tissue. Histopathological, biochemical and apoptotic findings show that silymarin has a protective effect against nephrotoxicity and hepatotoxicity caused by tacrolimus.

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Hepato-renal and hematological effects of flunixin and silymarin coadministration in rats

Cited by 7 publications

References 20 publications

Development of an experimental hepatic encephalopathy in a rabbit model: Biochemical and immunohistochemical study

Development of an experimental hepatic encephalopathy in a rabbit model: Biochemical and immunohistochemical study

Histopathological evaluation of lesions induced by dimethyl hydrazine in male rats

Protective effect of silymarin on tacrolimus-induced kidney and liver toxicity

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