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Saikosaponin‐b2 (SS‐b2), an active ingredient derived from the root of Radix Bupleuri, possesses antitumour, anti‐inflammatory, antioxidative and hepatoprotective properties. We investigated the inhibition of tumour proliferation by SS‐b2 and the underlying molecular mechanisms, including the MACC1/p‐c‐Met/p‐Akt pathway expression in HepG2 liver cancer cells and H22 tumour‐bearing mice. Animal experiments showed that SS‐b2 significantly decreased the levels of MACC1, p‐c‐MET and p‐Akt in tumour tissue transplanted with H22 liver cancer cells in mice, while it increased the expression of p‐BAD. The results also revealed a concentration‐dependent suppression of MACC1, p‐c‐Met and p‐Akt expression in the SS‐b2 treatment group compared with the control group. Additionally, the suppression of MACC1 activation by SS‐b2 resulted in a reduction in the viability and proliferation of HepG2 liver cancer cells, and this reduction was comparable to that by doxorubicin (DOX). This suggests that SS‐b2 has significant efficacy in liver cancer, comparable to DOX. Meanwhile, Annexin V‐FITC/PI staining and western blot analysis of cleaved caspase 9 and cleaved caspase 3 demonstrated that SS‐b2 induced apoptosis of HepG2 liver cancer cells. These findings provide experimental evidence suggesting that SS‐b2 is a promising anticancer agent for liver cancer.
Saikosaponin‐b2 (SS‐b2), an active ingredient derived from the root of Radix Bupleuri, possesses antitumour, anti‐inflammatory, antioxidative and hepatoprotective properties. We investigated the inhibition of tumour proliferation by SS‐b2 and the underlying molecular mechanisms, including the MACC1/p‐c‐Met/p‐Akt pathway expression in HepG2 liver cancer cells and H22 tumour‐bearing mice. Animal experiments showed that SS‐b2 significantly decreased the levels of MACC1, p‐c‐MET and p‐Akt in tumour tissue transplanted with H22 liver cancer cells in mice, while it increased the expression of p‐BAD. The results also revealed a concentration‐dependent suppression of MACC1, p‐c‐Met and p‐Akt expression in the SS‐b2 treatment group compared with the control group. Additionally, the suppression of MACC1 activation by SS‐b2 resulted in a reduction in the viability and proliferation of HepG2 liver cancer cells, and this reduction was comparable to that by doxorubicin (DOX). This suggests that SS‐b2 has significant efficacy in liver cancer, comparable to DOX. Meanwhile, Annexin V‐FITC/PI staining and western blot analysis of cleaved caspase 9 and cleaved caspase 3 demonstrated that SS‐b2 induced apoptosis of HepG2 liver cancer cells. These findings provide experimental evidence suggesting that SS‐b2 is a promising anticancer agent for liver cancer.
Endothelial dysfunction, the earliest manifestation of atherosclerosis, can be initiated by both biochemicals and biomechanical forces. Atherosclerosis occurs predominantly at arterial branch points, arterial bifurcations and the curved segments of great arteries. These are the regions that blood flows turbulently. Turbulence promotes endothelial dysfunction by reducing shear stress upon endothelial cells. The endothelial glycocalyx mediates the effect of shear stress upon the endothelium. A mathematical analysis of cardiovascular hemodynamics demonstrates that fluid retention increases turbulence of blood flow. While there is no empirical data confirming this relationship, fluid retention is associated with adverse cardiovascular events. Every medical condition that causes fluid retention is associated with increased risk of both atherosclerotic cardiovascular disease and venous thromboembolic disease. In addition, most medications that cause fluid retention are associated with increased adverse cardiovascular effects. Calcium channel blockers (CCBs) and pioglitazone are exceptions to this generalization. Even though data regarding CCBs and pioglitazone contradict the hypothesis that fluid retention is a cardiovascular risk factor, these medications have favorable cardiovascular properties which may outweigh the negative effect of fluid retention. Determining whether or not fluid retention is a cardiovascular risk factor would require empirical data demonstrating a relationship between fluid retention and turbulence of blood flow. While this issue should be relevant to cardiovascular researchers, clinicians and patients, it is especially pertinent to the pharmaceutical industry. Four-dimensional magnetic resonance imaging and vector flow Doppler ultrasound have the capability to quantify turbulence of blood flow. These technologies could be utilized to settle the matter.
This study explores the effect of dietary along with Lactobacillus rhamnosus GG (LGG) powder on intestinal and liver damage in broiler chickens challenged by lipopolysaccharide (LPS). A total of 100 healthy 1-day-old Ross 308 broiler chickens were selected and randomly divided into two treatments: the control group and the LGG treatment group. There were five replicates for each group, with 10 chickens per replicate. The chickens in the control group were fed a basal diet, while LGG treatment was supplemented with 1,000 mg/kg LGG along with the basal diet. The experiment lasted 29 days, and the trial included two phases. During the first 27 days, the animals were weighed on the 14th and 27th days to calculate growth performance. Then, on day 29, 2 animals from each replicate were intraperitoneally injected with 1 mg/kg BW LPS, and another 2 animals were treated with an equal volume of saline. The chickens were slaughtered 3 h later for sampling and further analysis. (1) LGG addition to the diet did not affect growth performance, including average daily gain (ADG), average daily feed intake (ADFI), and feed-to-weight ratio (F/G) of broiler chickens; (2) LPS stimulation decreased villus height (VH), and caused oxidative stress and increased the amount of diamine oxidase (DAO) in plasma, and the relative expression of intestinal inflammation genes (interleukin-8 [IL-8], interleukin 1β [IL-1β], inducible nitric oxide synthase [iNOS], and tumor necrosis factor-α [TNF-α]) and the relative expression of liver injury genes (b-cell lymphoma 2 [BCL2], heat shock protein70 [HSP70], and matrix metallopeptidase 13 [MMP13]). (3) Supplementation of LGG increased VH and the relative expression of intestinal barrier genes (mucins 2 [Mucin2] and occludin [Occludin]) and decreased the amount of DAO in plasma and the relative expression of intestinal inflammatory factors (IL-8, iNOS, and IL-1β). LGG supplementation also increased the expression of liver injury-related genes (MMP13 and MMP9). In conclusion, LGG enhanced intestinal barrier function, improved intestinal morphology, and alleviated the intestines’ inflammatory response in LPS-stimulated broiler chicken, and it has a slightly protective effect on liver damage.
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