Selenium nanoparticles and quercetin suppress thioacetamide-induced hepatocellular carcinoma in rats: Attenuation of inflammation involvement.

The current study investigates the anti-inflammatory and hepatoprotective effects of selenium (Se) formulated as nanoparticles (SeNPs) and in combination with quercetin (QCT) against thioacetamide (TAA)-induced hepatocellular carcinoma (HCC) in rats. ​​​​​​Seventy-two male Sprague-Dawley rats were divided into six groups (n = 12). Three control groups; normal, SeNPs; group received SeNPs only and HCC; group received TAA. In addition, three preventive groups; SeNPs + TAA, QCT + TAA, and QCT + SeNPs + TAA. Induction of HCC was detected histopathologically and by the raise of the serum level of alpha-fetoprotein (AFP). Oxidative stress was evaluated by the hepatic levels of reduced glutathione (GSH), glutathione peroxidase (GPx), and malondialdehyde (MDA) spectrophotometrically. The oncogenic pathway of p53/ß-catenin/cyclin D1 was assessed by immunohistochemistry. The inflammatory markers; interleukin-33 (IL-33), IL-6, and IL-1ß were assessed by enzyme-linked immune sorbent assay. SeNPs prevented the elevation of serum AFP and hepatic IL-33, IL-1ß, and IL-6 in comparison to HCC or QCT + TAA groups. SeNPs + TAA exhibited a lower positive hepatic staining of p53, ß-catenin, and cyclin D1 in comparison to HCC or QCT + TAA groups. Moreover, SeNPs improved the overall oxidative balance indicated by low hepatic MDA and enhanced GSH and GPx when compared to HCC or QCT + TAA groups. ​​SeNPs alone and in combination with QCT were found to suppress the progression of HCC in rats via the enhancement of the oxidative stress and then inflammatory status and the prevention of the deregulation of the oncogenic axis pathway of p53/ß-catenin/cyclin D.

Lidocaine-prilocaine cream versus local infiltration anesthesia in pain relief during repair of perineal trauma after vaginal delivery: a systematic review and meta-analysis.

Background: Perineal trauma is a common problem that may affect women during vaginal delivery; this trauma can be either spontaneous (tear) or intentional (episiotomy). When repair of perineal trauma is required, adequate analgesics must be obtained. Topical products as lidocaine-prilocaine (EMLA) cream is one of the suggested methods, but still there is lack of evidence with regard to its efficacy and safety.Objective: The aim of this review is to assess the evidence of utilizing EMLA cream in comparison to local perineal infiltration anesthesia for pain control during perineal repair after vaginal delivery.Data sources: Medline, Embase, Dynamed Plus, ScienceDirect, TRIP database, ClinicalTrials.gov and the Cochrane Library were searched electronically from January 2006 to May 2018 for studies investigating the effect of lidocaine-prilocaine cream in relieving pain during repair of perineal trauma.Methods of study selection: All randomized controlled trials assessing effect of lidocaine-prilocaine cream versus local infiltration anesthesia in relieving pain during repair of perineal trauma were considered for this meta-analysis. Fifteen studies were identified of which four studies deemed eligible for this review. Quality and risk of bias assessment was performed for all studies.Data extraction: Two researchers independently extracted the data from the individual articles and entered into RevMan software. The weighted mean difference (WMD) and 95% confidence interval (CI) was calculated. Statistical heterogeneity between studies was assessed by the Higgins chi-square and (I2) statistics. When heterogeneity was significant, a random-effects model was used for meta-analysis. Otherwise, the fixed effect meta-analysis was used when there was no significant heterogeneity.Results: Pooled analysis of result in "pain score" was insignificant between the two groups (WMD -1.11; 95% CI (-2.55 to 0.33); p = .13). Furthermore, the use of additional analgesia showed no statistically significant difference between the two groups (WMD 1.34; 95% CI (0.66-2.71), p = .42). Regarding patient satisfaction, an overall analysis of three studies showed significant results favoring EMLA cream group users (WMD 4.65; 95% CI (1.96-11.03), p = .0005). The pooled analysis of the outcome "duration of repair" showed the significantly shorter duration of repair in EMLA cream users (n = 92) than local infiltration anesthesia (n = 95) (1.72 min; 95% CI (-2.76 to -0.67), p = .001).Conclusions: This meta-analysis suggests that topical lidocaine-prilocaine cream gives comparable results in reducing pain during perineal repair after vaginal delivery.

Herbal management of hepatocellular carcinoma through cutting the pathways of the common risk factors.

Hepatocellular carcinoma (HCC) is considered the most frequent tumor that associated with high mortality rate. Several risk factors contribute to the pathogenesis of HCC, such as chronic persistent infection with hepatitis C virus or hepatitis B virus, chronic untreated inflammation of liver with different etiology, oxidative stress and fatty liver disease. Several treatment protocols are used in the treatment of HCC but they also associated with diverse side effects. Many natural products are helpful in the co-treatment and prevention of HCC. Several mechanisms are involved in the action of these herbal products and their bioactive compounds in the prevention and co-treatment of HCC. They can inhibit the liver cancer development and progression in several ways as protecting against liver carcinogens, enhancing effects of chemotherapeutic drugs, inhibiting tumor cell growth and metastasis, and suppression of oxidative stress and chronic inflammation. In this review, we will discuss the utility of diverse natural products in the prevention and co-treatment of HCC, through its capturing of the common risk factors known to lead to HCC and shed the light on their possible mechanisms of action. Our theory assumes that shutting down the risk factor to cancer development pathways is a critical strategy in cancer prevention and management. We recommend the use of these plants side by side to recent chemical medications and after stopping these chemicals, as a maintenance therapy to avoid HCC progression and decrease its global incidence.

Elaeagnus angustifolia Plant Extract Inhibits Angiogenesis and Downgrades Cell Invasion of Human Oral Cancer Cells via Erk1/Erk2 Inactivation.

Oral cancer is a common malignancy in both men and women worldwide; this cancer is characterized by a marked propensity for invasion and spreading to local lymph nodes. On the other hand, Elaeagnus angustifolia (EA) is a medicinal plant that has been used for centuries for treating many human diseases in the Middle East. However, the effect of EA plant extract on human cancers especially oral has not been investigated yet. Thus, first we examined the outcome of EA flower extract on angiogenesis, using the chorioallantoic membrane (CAM) of the chicken embryo; we found that EA extract reduces blood vessel development of the CAM. Then, we investigated the effect of EA flower extract on selected parameters in FaDu and SCC25 oral cancer cell lines. Our results show that EA extract inhibits cell proliferation and colony formation, in addition to the initiation of S cell cycle arrest and reduction of G1/G2 phase. In parallel, EA extract provokes differentiation to an epithelial phenotype "mesenchymal-to-epithelial transition: MET" which is the opposite of "epithelial-to-mesenchymal transition, EMT": an important event in cell invasion and metastasis. Thus, EA plant extract causes a dramatic decrease in cell invasion and motility abilities of FaDu and SCC25 cancer cells in comparison with their controls. These changes are accompanied by an upregulation of E-cadherin expression. The molecular pathway analysis of the EA flower extract reveals that it can inhibit the phosphorylation of Erk1/Erk2, which could be behind the inhibition of angiogenesis, the initiation of MET event, and the overexpression of E-cadherin. Our findings indicate that EA plant extract can reduce human oral cancer progression by the inhibition of angiogenesis and cell invasion via Erk1/Erk2 signaling pathways.