Search

Background Alcohol consumption is the fourth leading cause of death and disability worldwide. Several cellular pathways contribute to alcohol-mediated tissue injury. Adipose tissue apart from functioning as an endocrine organ secretes several hormones and cytokines known as adipokines that are known to play a significant role in alcohol-induced tissue damage. This study was designed to test the efficacy of diallyl sulfide (DAS) in regulating the alcohol-induced outcomes on adipose tissue. Methods Male Wistar rats were fed with 36% Lieber–DeCarli liquid diet containing ethanol (EtOH) for 4 weeks. Control rats were pair-fed with isocaloric diet containing maltodextrin instead of EtOH. During the last week of feeding protocol, the EtOH-fed rat group was given 200 mg/kg body weight of DAS through diet. We also studied DAS effect on isolated human primary adipocytes. Viability of human primary adipocytes on DAS treatment was assessed by MTT assay. Malondialdehyde (MDA), a marker of oxidative stress, was measured by HPLC and the thiobarbituric acid method. Expression of inflammatory genes and lipogenic genes was studied by qRT-PCR and Western blotting. Serum inflammatory gene expression was studied by ELISA. Results Our study results showed that DAS could alleviate EtOH-induced expression levels of proinflammatory and endoplasmic reticulum (ER) stress genes and improve adipose tissue mass and adipocyte morphology in male Wistar rats fed Lieber–DeCarli diet containing 6% EtOH. Further, we showed that DAS reduced the expression of lipogenic genes and improved lipid accumulation and adipocyte mass in human primary adipocytes treated with EtOH. Subsequently, we also showed that oxidative stress, as measured by the changes in MDA levels, was reduced in both male Wistar rats and human primary adipocytes treated with EtOH plus DAS. Conclusions Our study results prove that DAS is effective in ameliorating EtOH-induced damage to adipose tissue as evidenced by the reduction brought about by DAS in oxidative stress, ER stress, and proinflammatory gene expression levels. DAS treatment also regulated lipogenic gene expression levels, thereby reducing free fatty acid release. In conclusion, this study has clinical implications with respect to alcohol-induced adipose tissue injury among alcohol users.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous collection of conditions characterized by irreversible expiratory airflow limitation. The disease is interspersed with exacerbations; periods of acute symptomatic, physiological, and functional deterioration. The present study was designed to investigate the role of X-ray cross-complementing group 1 (XRCC1) and apurinic/apyrimidinic endonuclease 1 (APE1) polymorphisms and the risk of COPD. Blood samples from 354 unrelated subject (age range 18-60 years; 156 with COPD, 198 healthy controls) were collected. Genomic DNA was isolated and genotyped for XRCC1 Arg399Gln and APE1 Asp148Glu using a confronting two pair primers polymerase chain reaction. GA genotype of XRCC1 gene was found to be predominant in the COPD group compared to controls with 1.86-fold increased risk for COPD (OR 1.86, 95 % CI 1.20-2.88, p = 0.0013). TG genotype of APE1 was found to be predominant in COPD group compared to controls with the difference being statistically significant (OR 1.68, 95 % CI 1.08-2.61, p = 0.0043). The GA haplotype was found to be predominant in COPD than controls with a 2.19-fold significant increase (OR 2.19, 95 % CI 1.46-3.28, p = 0.003). Polymorphism in XRCC1 and APE1 gene is associated with an increased risk of COPD.

Liver transplant is considered is the only treatment for liver cirrhosis. Despite the success of organ transplantation, the treatment requires lifelong immunosuppression and major limitation is the availability of donor liver. Hepatic progenitor cell transplantation (HSCT) offers novel but challenging alternatives therapy to liver transplantation for management of liver cirrhosis. In this study, we investigated the cellular immune response by monitoring T-cell, NK-cell and cytokines which play major role in cellular rejection. A total of 5 patients with decompensated liver cirrhosis were enrolled in the study. T-cell (CD3, CD4 and CD8), NK-cells (CD16) was monitored before (Day-1) and after transplantation (Day 1, 7, 15, 30) of human fetal liver-derived EPCAM+Ve cell by flowcytometry. Before and after transplantation, Cytokinelevels (IL2, TNFβ, IFNα, IFNγ and INFβ) were also measured by ELISA. Study has demonstrated that after HSCT patient showed marked clinical recovery and decline in the MELD score and there was no significant increase found in cell mediated response and cytokine levels between pre and post transplantation. Hence this preliminary study demonstrated human fetal liver- derived EPCAM+Ve stem cell transplantation is safety for end stage liver cirrhosis.