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Cardiac hypertrophy is one of the key structural changes that occurs in diabetic cardiomyopathy. Previous studies have indicated that the activation of NF-κB by calpain-1, a Ca2+-dependent cysteine protease, serves an important role in cardiac hypertrophy. The aim of the present study was to assess the effect of 30 and 60 mg/kg Lycium barbarum polysaccharide (LBP) treatment, the major active ingredient extracted from Lycium barbarum, on cardiac hypertrophy in streptozotocin (STZ) induced diabetic rats. In addition, the present study examined the possible underlying mechanisms of this effect by assessing calpain-1 expression and the NF-κB pathway. The mRNA expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was determined by reverse transcription-quantitative PCR. Western blotting was used to detect the protein expressions of calpain-1, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and toll-like receptor-4 (TLR-4) in the heart tissue. The results revealed that compared with non-diabetic rats, diabetic rats exhibited cardiac hypertrophy. Cardiac hypertrophy was defined by the following: Dysfunction of the cardiac hemodynamics, an increase in the ratios of left ventricular weight/body weight and heart weight/body weight and the increased expressions of ANP and BNP, which serve as hypertrophic markers in cardiac tissue. However, all of these changes were attenuated in diabetic rats treated with LBP. In addition, the protein expression of calpain-1 was increased in the heart tissue of diabetic rats compared with that of non-diabetic rats, where it was inhibited by LBP. LBP also decreased the protein expression of certain inflammatory mediators, IL-6, TNF-α, ICAM-1, VCAM-1 and TLR-4 in diabetic heart tissue. Furthermore, LBP treatment reduced the production of reactive oxygen species, upregulated the protein expression of endothelial nitric oxide synthase and downregulated the protein expression of inducible nitric-oxide synthase. Additionally, LBP increased the protein expression of p65, the subunit of NF-κB and inhibitory protein кB-α in the cytoplasm and reduced p65 expression in the nucleus. In conclusion, LBP improves cardiac hypertrophy, inhibits the expression of calpain-1 and inhibits the activation of NF-κB in diabetic rats. [ABSTRACT FROM AUTHOR]

Hepatitis B cirrhosis is caused by liver cell necrosis, residual liver cell nodular regeneration, connective tissue hyperplasia and fiber formation, which frequently leads to adrenal insufficiency. Previous reports have demonstrated that human fibroblast growth factor (hFGF)‑21 is a multifunctional protein that exhibits potential therapeutic value for metabolic diseases. The present study investigated the diagnostic value of hFGF‑21 and analyzed the potential molecular mechanism in the progression of hepatitis B cirrhosis combined with adrenal insufficiency. Characteristics of cellular immunity and humoral immunity were analyzed in patients with hepatitis B cirrhosis combined with adrenal insufficiency (PhbA). Results demonstrated that expression levels of hFGF‑21 were downregulated in plasma and liver cells isolated from clinical specimens. Plasma concentration levels of hFGF‑21 were upregulated in prognostic PhbA. In vitro assays indicated that hFGF‑21 treatment decreased the continuous deposition of extracellular matrix and reactive oxygen species in liver cells isolated from clinical specimens. Results also demonstrated that hFGF‑21 treatment downregulated inflammatory cytokines. It was observed that hFGF‑21 treatment downregulated nuclear factor (NF)‑κB and Kruppel‑like factor 6. Notably, transforming growth factor (TGF)‑β, platelet‑derived growth factor and epidermal growth factor levels were improved by hFGF‑21 treatment. In conclusion, these results indicated that hFGF‑21 inhibits inflammation by regulation of the NF‑κB‑mediated TGF‑β signaling pathway, which may serve as a predictor and prognostic factor in PhbA. [ABSTRACT FROM AUTHOR]

The study assessed the correlation between cortisol (COR) levels and concurrent infection for the patients with hepatitis B cirrhosis for corresponding countermeasure analysis. In total, 86 patients with hepatitis B cirrhosis (non‑infection group) and 32 patients with hepatitis B cirrhosis complicated with infection (infection group) who were diagnosed and treated in the Beijing YouAn Hospital from March 2014 to March 2017 were selected. The fasting venous blood of all the patients was drawn to detect COR, cortisol binding globulin (CBG), blood routine indexes, C-reactive protein (CRP), procalcitonin (PCT), endotoxin and other indicators. The relative expression of CBG mRNA was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The differences and correlation of COR levels between the infection and non-infection groups were compared and analyzed. The concentrations of COR and CBG were decreased with the increase of Child‑Pugh grade, and the difference was statistically significant (P<0.05). COR, CBG and free cortisol (FC) concentrations with the same Child‑Pugh grade in the non-infection group were higher than those in the infection group (P<0.05). COR, CBG and FC concentrations of abdominal infection complicated with sepsis or abdominal infection complicated with pulmonary infection were lower than those of simple abdominal infection (P<0.05). The relative expression of CBG mRNA was detected by RT-qPCR, which also showed that: for Child-Pugh grade, grade A > grade B > grade C (P<0.05), non-infection group > infection group (P<0.05), abdominal infection + sepsis group and abdominal infection + pulmonary infection group were lower than the simple abdominal infection group (P<0.05). The values of white blood cells (WBC), neutrophils, CRP, PCT and endotoxin in the infection group were higher than those in the non-infection group, and the differences were statistically significant (P<0.05). COR, CGB and FC were negatively correlated with inflammatory indexes such as WBC, neutrophils, CRP, PCT and endotoxin. The r value of COR and FC in the non-infection group was 0.678, while that of OR and FC in the infection group was 0.787. COR was positively correlated with FC before and after infection. The results of the study show that the cortisol levels of patients with hepatitis B cirrhosis are significantly correlated with whether infected or not, levels of disease condition and infection types, and can be used as sensitive indicators of hepatitis B cirrhosis infection. [ABSTRACT FROM AUTHOR]