Antitumor effect of matrine in human hepatoma G2 cells by inducing apoptosis and autophagy. Zhang Jun-Qiang,Li Yu-Min,Liu Tao,He Wen-Ting,Chen Ying-Tai,Chen Xiao-Hui,Li Xun,Zhou Wen-Ce,Yi Jian-Feng,Ren Zhi-Jian World journal of gastroenterology AIM:To study the antitumor effect of matrine in human hepatoma G2 (HepG2) cells and its molecular mechanism involved in antineoplastic activities. METHODS:3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect viability of HepG2 cells. The effect of matrine on cell cycle was detected by fl ow cytometry. Annexin-V-FITC/PI double staining assay was used to detect cellular apoptosis. Cellular morphological changes were observed under an inverted phase contrast microscope. Transmission electron microscopy was performed to further examine ultrastructural structure of the cells treated with matrine. Monodansylcadaverine (MDC) staining was used to detect autophagy. Whether autophagy is blocked by 3-methyladenine (3-MA), an autophagy inhibitor, was evaluated. Expression levels of Bax and Beclin 1 in HepG2 cells were measured by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS:Matrine significantly inhibited the proliferation of HepG2 cells in a dose- and time-dependent manner, and induced G1-phase cell cycle arrest and apoptosis of HepG2 cells in a dose-dependent manner. The total apoptosis rate was 0.14% for HepG2 cells not treated with matrine. In contrast, the apoptosis rate was 28.91%, 34.36% and 38.80%, respectively, for HepG2 cells treated with matrine at the concentration of 0.5, 1.0 and 2.0 mg/mL. The remarkable morphological changes were observed under an inverted phase contrast microscope. Abundant cytoplasmic vacuoles with varying sizes were observed in HepG2 cells treated with matrine. Furthermore, vacuolization in cytoplasm progressively became larger and denser when the concentration of matrine was increased. Electron microscopy demonstrated formation of abundant autophagic vacuoles in HepG2 cells after matrine treatment. When the specific autophagic inhibitor, 3-MA, was applied, the number of autophagic vacuoles greatly decreased. MDC staining showed that the fluorescent density was higher and the number of MDC-labeled particles in HepG2 cells was greater in matrine treatment group than in control group. Fewer autophagic vacuoles were observed in the combined 3-MA and matrine treatment group when 3-MA was added before matrine treatment, indicating that both autophagy and apoptosis are activated when matrine-induced death of hepatoma G2 cells occurs. Real-time quantitative RT-PCR revealed that the expression levels of Bax gene, an apoptosis-related molecule, and Beclin 1 gene which plays a key role in autophagy were higher in matrine treatment group than in control group, indicating that Beclin 1 is involved in matrine-induced autophagy and the pro-apoptotic mechanism of matrine may be related to its upregulation of Bax expression. CONCLUSION:Matrine has potent antitumor activities in HepG2 cells and may be used as a novel effective reagent in treatment of hepatocellular carcinoma. 10.3748/wjg.v16.i34.4281

Protective Effect of Poria Cocos Polysaccharides on Fecal Peritonitis-Induced Sepsis in Mice Through Inhibition of Oxidative Stress, Inflammation, Apoptosis, and Reduction of Treg Cells. Frontiers in microbiology This study was conducted to investigate the potential pharmacological effects of Poria cocos polysaccharides (PCPs) on fecal-induced peritonitis (FIP) mice. Consequently, the fecal peritonitis (FP)-induced septic mice with the higher levels of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), IL-1β, malondialdehyde (MDA), myeloperoxidase (MPO), histopathological lesion and bacterial burden, and lower levels of superoxide dismutase (SOD) and glutathione (GSH). Interestingly, PCP pre-treatment reduced inflammatory cytokines and oxidative stress in plasma and spleen and improved the resistance to FIP. Inflammatory infiltration and cell death in thymus or splenic tissue were alleviated with PCP pretreatment. Furthermore, Treg cells were moderated in the spleen with PCP pre-administration. In addition, PCP pretreatment downregulated Annexin-V in the thymus of FP-induced septic mice, and apoptosis of splenic cells was dose-dependent. In conclusion, PCPs have pharmacological and biological effects on FP-induced septic mice, and its molecular mechanism is related to antioxidative, anti-inflammation, anti-apoptosis, and the reduction of Treg activity in splenic cells. 10.3389/fmicb.2022.887949

Research Note: Poria cocos polysaccharide alleviates lipopolysaccharide-induced intestinal inflammation and barrier damage in broiler chickens. Poultry science This study aimed to explore the impact of dietary supplementation of Poria cocos polysaccharide (PCP) on the lipopolysaccharide(LPS)-induced intestinal inflammation, morphology, and barrier damage in broilers. A total of 240 1-day-old male Arbor Acre broilers were randomly divided into 4 groups in a 2 × 2 factorial design comprising PCP supplementation (0 or 2 g/kg PCP from d 1 to 23) and LPS challenge (intraperitoneal injection of 1.5 mg/kg body weight of LPS or the same volume of sterile saline at d 22). Our results showed that compared to the non-LPS-treated groups, the treated birds showed a decrease in the ADG, VH, V/C, and the expression of ZO-1, occludin, claudin 1, and mucin2 in the duodenum and jejunum (P < 0.05). However, dietary PCP supplementation significantly mitigated these effects (P < 0.05) except for mucin2 in the duodenum. Furthermore, LPS treatment increased the levels of sIgA and upregulated the mRNA abundances of IL-1β, IL-6, TNF-α, IFN-γ, TLR-4, and MyD88 both in the duodenal and jejunal mucosa (P < 0.05). Whereas, PCP supplementation significantly reversed the LPS-induced effects on these genes (P < 0.05) except for the TLR-4 and MyD88. However, LPS did not impact the expression of anti-inflammatory IL-10 in the duodenal and jejunal mucosa (P > 0.05). Briefly, this study implied that dietary PCP supplementation could ameliorate intestinal inflammation and mucosal damage of LPS-challenged broilers, improving broiler performance. 10.1016/j.psj.2024.104126