Serum levels of bcl-2 and cellular oxidative stress in patients with viral hepatitis

Osman, H. G.; Gabr, OM; Lotfy, S; Gabr, Sami A.

doi:10.4103/0255-0857.37333

Cited by 35 publications

(15 citation statements)

References 17 publications

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“…These studies mostly measured MDA as an oxidation marker, which was significantly higher in patients with hepatitis B infection compared to healthy individuals (Table 1); a marker that was positively correlated to alanine aminotransferase (ALT) (23-25, 30, 31, 41), HBV-DNA (23, 32), total and direct bilirubin (28), serum bcl-2 (this study combined hepatitis B and C patients) (47), gamma-glutamyl transpeptidase (GGT) (31), serum iron/ferritin (44), and liver ultrasonography findings (coarse texture) (28) in some studies. Although another study demonstrated a significant increase in the MDA levels of chronic hepatitis B patients, it did not find a significant difference between inactive HBsAg carriers and controls (48).…”

Section: Resultsmentioning

confidence: 99%

Hepatitis B and its Relationship With Oxidative Stress

Alavian

Showraki

2016

Hepat Mon

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ContextDespite the great breakthroughs we have witnessed in the last 50 years in the prevention, diagnosis, and treatment of hepatitis B, we are still far from eradicating or even curing the disease. Achieving further progress in controlling this disease will not be possible without discovering the exact pathogenesis behind it. One prime suspect in the pathogenesis of various diseases is oxidative stress. This review will exclusively explore hepatitis B in the context of oxidative stress to obtain a more comprehensive clinical perspective on its pathogenesis and eventual medical therapy.Evidence AcquisitionWe systematically searched PubMed, Google Scholar, Web of Science, EMBASE, and Scopus using an extensive list of keywords in the following three categories: 1) Hepatitis B and oxidation 2) Hepatitis B and antioxidant system 3) Effects of approved anti-hepatitis B drugs on redox status. All relevant articles were obtained and reviewed carefully after the exclusion criteria were deployed.ResultsThere is great evidence indicating extensive oxidative stress occurs in hepatitis B. This oxidative stress takes place on multiple levels, including lipid peroxidation, DNA oxidation, protein oxidation, and reactive oxygen and nitrogen species production. However, there are also conflicting results with regard to antioxidant therapy and antioxidant status in hepatitis B, some of which may be explained by the concept of “compensatory gaps.” Nevertheless, further studies are indicated to reach a more thorough judgment.ConclusionsDespite the presence of vast oxidative stress in hepatitis B, antioxidant therapy is not always effective as a treatment strategy, especially considering that antioxidants can act as “double-edged swords” or antioxidants; if not used at the right time or place or in the right combination, these substances can easily become pro-oxidants. Therefore, several studies will be needed to determine suitable antioxidant therapies. We propose the “2-step Combined Antioxidant Adjuvant Therapy for hepatitis B (2CAAT Hep B)” as a new strategy for antioxidant adjuvant therapy. We also suggest developing an international platform and database for antioxidant adjuvant therapy in hepatitis B (IPAATH and IDAATH) to canalize this field of research in a standardized direction, especially when complexity is a problem.

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Section: Resultsmentioning

confidence: 99%

Hepatitis B and its Relationship With Oxidative Stress

Alavian

Showraki

2016

Hepat Mon

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“…It is likely that in the initial phase, apoptosis also acts on activated HSCs, decreasing the collagen fibres. Osman et al (2007) demonstrated a close link between serum levels of Bcl-2 and cellular oxidative stress in patients with viral hepatitis. Nakamoto et al (2002) revealed the involvement of Bcl-2 in HCV pathogenesis and demonstrated that the abnormality of peripheral blood mononuclear cells subsets in undergoing apoptosis as a result of the down-regulation of Bcl-2 expression may contribute to viral persistence and progression of liver disease in chronic hepatitis C.…”

Section: Fig 4 (A-i) Photomicrographs Of Liver Sections From (A) Comentioning

confidence: 92%

Hepatoprotective effects of early pentoxifylline administration on hepatic injury induced by concanavalin A in rat

Mohamed

Elmelegy

El-Aziz

et al. 2014

Can. J. Physiol. Pharmacol.

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Tumor necrosis factor alpha (TNF-α) plays an important role in the pathogensis of hepatitis C virus (HCV) infection induced liver injury. This study aimed to evaluate the effects of TNF-α inhibition with pentoxifylline (PTX) on concanavalin A (Con A)-induced hepatic injury in rats. The rats were distributed among 3 groups: (i) control group (1 mL saline·week(-1) by intravenous injection (i.v.)); (ii) Con A treatment group (20 mg Con A·(kg body mass)(-1)·week(-1), i.v.), and (iii) rats treated with Con A and with PTX (200 mg PTX·(kg body mass)(-1)·day(-1), per oral) group. Blood samples and livers were collected at the end of weeks 1, 2, 4, and 8 of Con A treatment. Portal pressure (PP) was measured at the end of week 8. The administration of PTX was found to confer significant protection against the injurious effects of Con A on the liver, by reducing serum levels of aspartate aminotransferase, alanine aminotransferase, hepatic TNF-α, and malondialdehyde. Histopathological examination revealed that treatment with PTX significantly suppressed early inflammation, reduced alpha smooth muscle actin, and the apoptosis of hepatocytes induced by Con A. Moreover, PTX significantly (P < 0.05) reduced PP, and quantitative analyses of the area of fibrosis induced by treatment with Con A showed a significant reduction at the end of week 8. We conclude that rats treated with PTX revealed a more or less normal hepatocyte architecture as well as marked improvement in fibrosis and PP.

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“…[22] Serum Bcl-2 level was measured in patients with viral hepatitis; the data obtained showed a significantly elevated Bcl-2 level in the serum of liver cancer as compared to cirrhosis and chronic cases. [23] In addition, a recent study on psoriatic patients showed that there is no difference in the level of serum Bcl-2 before and after topical treatment and no significant difference between patients with mild and severe psoriasis was reported. [24] The exact source of these apoptosis-regulating proteins in the blood of the patients is not known.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis and clinical severity in patients with psoriasis and HCV infection

Gabr

Berika²,

Alghadir

2014

Indian J Dermatol

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Background:It has been proposed that hepatitis C virus (HCV) antigens are involved in the pathogenesis of psoriasis and may contribute to severity of the disease. Increased expression of the apoptosis-regulating proteins p53 and tTG and decreased levels of bcl-2 in the keratinocytes of the skin of psoriatic patients have been reported.Aim:This study aims to identify the serum levels of apoptosis-regulating proteins in patients with psoriasis and without HCV infection and to study the relation between clinical severity of psoriasis and the presence of HCV infection.Materials and Methods:Disease severity was assessed by psoriasis area severity index score (PASI) of 90 patients with psoriasis grouped as mild (n = 30), moderate (n = 30) and severe (n = 30); 20 healthy individuals were used as controls. All groups were subjected for complete history taking, clinical examination, and tests for liver function and HCV infection. The serum levels of apoptosis related proteins: p53, tTG and bcl-2 were estimated by enzyme linked immune sorbent assay (ELISA).Results:There was a statistically significant (P < 0.001) correlation between clinical severity of psoriasis and presence of HCV antibodies and HCV-mRNA. In addition, significantly (P < 0.001) raised serum p53 and tTG, and reduced bcl-2 were observed among HCV-positive patients as compared to HCV-negative patients and control patients.Conclusion:These results conclude that clinical severity of psoriasis is affected by the presence of HCV antibodies and overexpression of apoptotic related proteins. In addition, altered serum levels of apoptosis-regulating proteins could be useful prognostic markers and therapeutic targets of psoriatic disease.

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Serum levels of bcl-2 and cellular oxidative stress in patients with viral hepatitis

Cited by 35 publications

References 17 publications

Hepatitis B and its Relationship With Oxidative Stress

Hepatitis B and its Relationship With Oxidative Stress

Hepatoprotective effects of early pentoxifylline administration on hepatic injury induced by concanavalin A in rat

Apoptosis and clinical severity in patients with psoriasis and HCV infection

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