A comprehensive systematic review of the literature was conducted on parameters from ¹⁸ F-FDG PET and a meta-analysis of the prognostic value of the maximal standard uptake value (SUVmax), metabolic tumor volume (MTV) and total lesional glycolysis (TLG) in patients with breast cancer (BC). Relevant English articles from PubMed, EMBASE, and the Cochrane Library were retrieved. Pooled hazard ratios (HRs) were used to assess the prognostic value of SUVmax, MTV, and TLG. A total of 20 primary studies with 3115 patients with BC were included. The combined HRs (95% confidence interval [CI] of higher SUVmax and higher TLG for event-free survival (EFS) were 1.53 (95% CI, 1.25–1.89, P = 0.0006) and 5.94 (95% CI, 2.57–13.71, P = 0.97), respectively. Regarding the overall survival (OS), the combined HRs were 1.22 (95%CI, 1.02–1.45, P = 0.0006) with higher SUVmax, and 2.91(95% CI, 1.75–4.85, P = 0.44) with higher MTV. Higher MTV showed no correlation with EFS [1.31(95% CI, 0.65–2.65, P = 0.18)] and similarly higher TLG showed no correlation with OS [1.20(95% CI, 0.65–2.23, P = 0.45)]. Subgroup analysis showed that SUVmax, with a median value of 5.55 was considered as a significant risk factor for both EFS and OS in BC patients. Despite clinically heterogeneous BC patients and adoption of various methods between studies, the present meta-analysis results confirmed that patients with high SUVmax are at high risk of adverse events or death in BC patients, high MTV predicted a high risk of death and high TLG predicted a high risk of adverse events.

Salidroside (SAL), a phenylpropanoid bioactive compound, has various pharmacological properties, including antioxidant, anti-inflammatory, and hepatoprotective effects. However, the pharmacological effects and mechanisms of action of SAL on cholestatic liver injury are unclear. This study investigated the mechanism and effects of salidroside (SAL) on intestinal flora distribution and hepatic stellate cell (HSC) activation in cholestatic hepatic fibrosis. Bile duct ligation was used to cause cholestasis BALB/c mice. The therapeutic efficacy of SAL in liver fibrosis was assessed via serum/tissue biochemical analyses and liver tissue hematoxylin and eosin and Masson staining. Inflammation and oxidative stress were analyzed using enzyme-linked immunosorbent assay and western blotting. HSC were activated in vitro using lipopolysaccharide, and the effects of SAL on HSC migration and inflammatory factor expression were detected via scratch, transwell, and western blotting assays. The effects of SAL on the PI3K/AKT/GSK-3β pathway in vivo and in vitro were detected using western blotting. 16sRNA sequencing was used to detect the effect of SAL on the diversity of the intestinal flora. Ileal histopathology and western blotting were used to detect the protective effect of SAL on the intestinal mucosal barrier. SAL reduces liver inflammation and oxidative stress and protects against liver fibrosis with cholestasis. It inhibits HSC activation and activates the PI3K/AKT/GSK-3β pathway in vitro and in vivo. Additionally, SAL restores the abundance of intestinal flora, which contributes to the repair of the intestinal mucosal barrier, inhibits endotoxin translocation, and indirectly inhibits HSC activation, reversing the course of cholestatic liver fibrosis. SAL inhibits HSC activation through the PI3K/AKT/GSK-3β pathway and improves intestinal flora distribution, thereby protecting and reversing the progression of hepatic fibrosis.