Dyslipidemia is an important and common cardiovascular risk factor in the general population. The lipid-lowering effects of turmeric and curcumin are unconfirmed. We performed a meta-analysis to assess the efficacy and safety of turmeric and curcumin in lowering blood lipids in patients at risk of cardiovascular disease (CVD). A comprehensive literature search was conducted on PubMed, Embase, Ovid, Medline and Cochrane Library databases to identify randomized controlled trials (published as of November 2016) that assessed the effect of turmeric and curcumin on blood lipid levels including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Pooled standardized mean difference (SMD) with 95% confidence interval (CI) was used to assess the effect. The analysis included 7 eligible studies (649 patients). Turmeric and curcumin significantly reduced serum LDL-C (SMD = −0.340, 95% confidence interval [CI]: −0.530 to −0.150, P < 0.0001) and TG (SMD = −0.214, 95% CI: −0.369 to −0.059, P = 0.007) levels as compared to those in the control group. These may be effective in lowering serum TC levels in patients with metabolic syndrome (MetS, SMD = −0.934, 95% CI: −1.289 to −0.579, P < 0.0001), and turmeric extract could possibly have a greater effect on reducing serum TC levels (SMD = −0.584, 95% CI: −0.980 to −0.188, P = 0.004); however, the efficacy is yet to be confirmed. Serum HDL-C levels were not obviously improved. Turmeric and curcumin appeared safe, and no serious adverse events were reported in any of the included studies. Turmeric and curcumin may protect patients at risk of CVD through improving serum lipid levels. Curcumin may be used as a well-tolerated dietary adjunct to conventional drugs. Further research is required to resolve uncertainties related to dosage form, dose and medication frequency of curcumin.

Background: Nonalcoholic fatty liver disease (NAFLD) has become prevalent in recent decades, especially in developed countries, and approaches for the prevention and treatment of NAFLD are not clear. The aim of this research was to analyze and summarize randomized controlled trials that investigated the effects of probiotics on NAFLD. Methods: Seven databases (PubMed, Embase, the Web of Science, the Cochrane Library, China National Knowledge Infrastructure, Wan Fang Data, and VIP Database) were searched. Then, eligible studies were identified. Finally, proper data extraction, synthesis and analysis were performed by trained researchers. Results: Anthropometric parameters: with use of probiotics weight was reduced by 2.31 kg, and body mass index (BMI) was reduced by 1.08 kg/m². Liver function: probiotic treatment reduced the alanine aminotransferase level by 7.22 U/l, the aspartate aminotransferase level by 7.22 U/l, the alkaline phosphatase level by 25.87 U/l, and the glutamyl transpeptidase level by −5.76 U/l. Lipid profiles: total cholesterol, low-density lipoprotein cholesterol, and triglycerides were significantly decreased after probiotic treatment. Their overall effects (shown as standard mean difference) were −0.73, −0.54, and −0.36, respectively. Plasma glucose: probiotics reduced the plasma glucose level by 4.45 mg/dl and the insulin level by 0.63. Cytokines: probiotic treatment decreased tumor necrosis factor alpha by 0.62 and leptin by 1.14. Degree of liver fat infiltration (DFI): the related risk of probiotics for restoring DFI was 2.47 (95% confidence interval, 1.61–3.81, p < 0.001). Conclusion: Probiotic treatment or supplementation is a promising therapeutic method for NAFLD.

Hepatocellular carcinoma is the second most common cause of cancer-related deaths worldwide. Due to a high propensity to metastasize, active angiogenesis and rapid proliferation, recurrence and poor prognosis are major obstacles for treatment and cure of this disease. However, the detailed mechanisms of how fatty acid synthase (FASN) promotes migration, invasion and healing in tumor cells remain unclear. In the present study, the previous results that FASN was expressed higher in cancer samples than in non-cancerous samples, and influenced migration, invasion of hepatoma carcinoma cells, were verified by immunohistochemistry, tissue microarrays, Transwell assay and wound healing assay. The secretory proteins of hepatocellular carcinoma cells with or without FASN knockdown were analyzed using the isobaric tags for relative and absolute quantitation (iTRAQ) method to identify differentially expressed proteins (DEPs). The DEPs were verified by RT-PCR and western blot analysis, and were consistent with the iTRAQ results. Inhibition of FASN can decrease the levels of IGFBP1, and the expression, activity, and ubiquitination of HIF-1α. Inhibition of FASN can suppress migration, invasion and healing of hepatoma carcinoma cells by decreasing HIF-1α, and IGFBP1.