Anti-Human BAX (Phospho-Thr167) polyclonal antibody

Obesity-induced adipocyte apoptosis promotes inflammation and insulin resistance. Src homology domain-containing inositol 5 '-phosphatase 1 (SHIP1) is a key factor of apoptosis and inflammation. However, the role of SHIP1 in obesity-induced adipocyte apoptosis and autophagy is unclear. We found that diet-induced obesity (DIO) mice have significantly greater crown-like structures and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL)-positive cells than ob/ob or control mice. Using RNA sequencing (RNA-seq) analysis, we identified that the apoptosis- and inflammation-related gene Ship1 is upregulated in DIO and ob/ob mice compared with control mice. In particular, DIO mice had more SHIP1-positive macrophages and lysosomal-associated membrane protein 1 (LAMP1) as well as a higher B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax)/Bcl-2 ratio compared with ob/ob or control mice. Furthermore, caloric restriction attenuated adipose tissue inflammation, apoptosis, and autophagy by reversing increases in SHIP1-associated macrophages, Bax/Bcl2-ratio, and autophagy in DIO and ob/ob mice. These results demonstrate that DIO, not ob/ob, aggravates adipocyte inflammation, apoptosis, and autophagy due to differential SHIP1 expression. The evidence of decreased SHIP1-mediated inflammation, apoptosis, and autophagy indicates new therapeutic approaches for obesity-induced chronic inflammatory diseases.

To investigate the effects and potential mechanisms of dietary choline on apoptosis in the gill of juvenile grass carp (Ctenopharyngodon idella), fish were fed diets containing different levels of choline (142.2, 407.4, 821.6, 1215.8, 1589.3, and 1996.6 mg kg(-1)) for 70 days, then sampled after a 3-days challenge test. The results revealed that optimal choline supplementation (1) reduced the incidence of rotten gill and protected gill morphology; (2) increased the contents of choline, acetylcholine, betaine, and phosphatidylcholine in grass crap gill; (3) reduced the proportion of positive cells with TUNEL assay and the degree of DNA fragments. Similarly, down-regulated the activities of caspase-3, -8, -9. Reduced caspase-3, -7, -8, -9, Bcl-2 associated X protein (Bax), Fas ligand (FASL), p38MAPK, and apoptotic protease activating factor-1(Apaf1) mRNA levels, as well as cytochrome C (CtyC) protein level. Up-regulated myeloid cell leukemia-1 (Mel-1) and the inhibitor of apoptosis protein (IAP) mRNA level in grass carp gill, suggested that choline inhibited cell apoptosis in fish gill; (4) decreased p-p38MAPK, T-p38MAPK protein levels and down-regulated the JAK2,TYK2, and STAT3 mRNA levels, as well as p-STAT3 protein abundance in grass crap gill, indicating that choline protected cell apoptosis in association with p38MAPK and JAK1(TYK2)/STAT3 signalling pathways in fish gill; In conclusion, choline protected the gill health and inhibited gill apoptosis might be related to p38MAPK and JAK1(TYK2)/STAT3 signalling pathways in fish. Moreover, the requirements of choline for resist gill rot morbidity and apoptosis indices (DNA fragmentation) of grass carp (9.28-108.97 g) were calculated as 1548.07 and 1383.20 mg kg(-1) diet, respectively.