Polygoni multiflori radix exacerbates idiosyncratic inflammatory liver injury through the FXR-SHP pathway and altered pharmacokinetic behavior.

Polygoni multiflori radix (PM) is a well-known tonic herb. It has been reported that PM could cause idiosyncratic inflammatory liver injury in some individuals. In this study, we investigated the mechanism of PM-induced idiosyncratic inflammatory liver injury in zebrafish and rat models based on pharmacodynamics and pharmacokinetics. The zebrafish were administered with polygoni multiflori radix extract (PME), emodin (EMO), and 2,3,5,4'-tetrahydroxystilbene-2-Ο-ß-D-glucoside (TSG) after lipopolysaccharide (LPS) treatment, to establish an idiosyncratic inflammation model. In zebrafish with idiosyncratic inflammation, PME, EMO, and TSG decreased liver area and brightness and increased the number of immune cells around the colliculi. PME+LPS produced hepatocyte damage, aggravated mitochondrial and endoplasmic reticulum damage, and increased AST and ALT activity. RT-PCR showed that PME and EMO up-regulated the expression of IL-6, IL-1ß, and INF-γ, and PME down-regulated expression of FXR and SHP. In rats with idiosyncratic inflammation, AST and ALT activities increased significantly, and liver tissues showed pathological damage. An efficient and sensitive LC-MS/MS method was established for the pharmacokinetic study of EMO and TSG in rats with idiosyncratic inflammation. The AUC0-t was higher for EMO and TSG in the model group compared with the normal group. The MRT0-t was significantly prolonged in EMO, while CLz/F was significantly reduced. The present results suggested that the absorption of potentially toxic components of PM increased and metabolism slowed down under inflammatory stress, and PM induced idiosyncratic liver injury via the FXR-SHP axis.

Nasal colonization of Staphylococcus aureus and the risk of surgical site infection after spine surgery: a meta-analysis.

BACKGROUND CONTEXT: Nasal colonization of Staphylococcus aureus may increase the risk of surgical site infection (SSI) after spine surgeries, although the results of previous studies were inconsistent. PURPOSE: To evaluate the influences of nasal colonization of S. aureus, methicillin-susceptible SA, and methicillin-resistant SA (MRSA) on the incidence of SSI after spine surgery. STUDY DESIGN/SETTING: Systematic review and meta-analysis. PATIENT SAMPLE: Seven studies including 10,650 patients who underwent nasal swab examination before spine surgeries were included, and 221 patients had nasal colonization of MRSA at baseline. OUTCOME MEASURES: Association between baseline nasal colonization of S. aureus, MRSA, and SSI after spine surgery. METHODS: Relevant follow-up studies were identified through systematic searches of the PubMed, Embase, and Cochrane Library databases. A random effects model was applied to pool the results. Subgroup analyses were performed according to whether MRSA decolonization was applied. RESULTS: During follow-up, a total of 244 SSI events occurred, including 57 MRSA-SSI events. Pooled results showed that nasal S. aureus (risk ratio [RR]=0.75, p=.22) or methicillin-susceptible SA colonization (RR=0.60, p=.22) did not significantly affect the risk of overall SSI after surgeries. However, nasal MRSA colonization was associated with significantly increased risks of overall SSI and MRSA-SSI (RR=2.52 and 6.21, respectively, both p<.001). Interestingly, the associations between nasal MRSA colonization and increased risks of overall and MRSA-SSI remained significant in studies without MRSA decolonization, but became insignificant in studies with MRSA decolonization. CONCLUSIONS: Nasal MRSA colonization may be associated with increased risks of overall SSI and MRSA-SSI after spine surgeries, and nasal MRSA decolonization may be associated with a reduction of SSI in these patients.