The antitumor effect of the combination of aconitine and crude monkshood polysaccharide on hepatocellular carcinoma.

Aconitine, the main component in Radix Aconiti Lateralis Preparata, not only exerts the anti-tumor effect on Hepatocellular Carcinoma (HCC) but also damages on immune system. In the present study, Crude Monkshood Polysaccharide (CMP), another one natural composition component originated from the same herbal with aconitine, combined with aconitine to investigate the effects on HCC and immunity in vitro and in vivo. The combination of CMP and aconitine enhanced the ability of the immunocyte to kill the tumor cell in vitro and had an additive effect on anti-HCC in vivo. Aconitine-CMP in combination improved the spleen weights, spleen index, thymus weights, thymus index. Elevated CD4+ T and CD8+ T cells and macrophages in spleen, decreased serum IL-6 level and increased serum IFN-γ and TNF-α levels were observed in mice treated with the combination of aconitine and CMP compare with control group (P<0.05). Our results showed that the combination of aconitine and CMP exerts anti-tumor effect by directly killing tumor cells and enhancing the anti-tumor immune responses, which further implies that chemotherapy drugs combined with Chinese medicine immunopotentiator maybe a feasible and effective strategy for HCC.

Frontline Science: Two flavonoid compounds attenuate allergic asthma by regulating epithelial barrier via G protein-coupled estrogen receptor: Probing a possible target for allergic inflammation.

Allergic asthma is a common chronic lung inflammatory disease and seriously influences public health. We aim to investigate the effects of formononetin (FMN) and calycosin (CAL), 2 flavonoids in Radix Astragali, on allergic asthma and elucidate possible therapeutic targets. A house dust mite (HDM)-induced allergic asthma mouse model and TNF-α and Poly(I:C) co-stimulated human bronchial epithelial cell line (16HBE) were performed respectively in vivo and in vitro. The role of G protein-coupled estrogen receptor (GPER) was explored by its agonist, antagonist, or GPER small interfering RNA (siGPER). E-cadherin, occludin, and GPER were detected by western blotting, immunohistochemistry, or immunofluorescence. The epithelial barrier integrity was assessed by trans-epithelial electric resistance (TEER). Cytokines were examined by enzyme-linked immunosorbent assay (ELISA). The results showed that flavonoids attenuated pulmonary inflammation and hyperresponsiveness in asthmatic mice. These flavonoids significantly inhibited thymic stromal lymphopoietin (TSLP), increased occludin and restored E-cadherin in vivo and in vitro. The effects of flavonoids on occludin and TSLP were not interfered by ICI182780 (estrogen receptor antagonist), while blocked by G15 (GPER antagonist). Furthermore, compared with PPT (ERα agonist) and DPN (ERß agonist), G1 (GPER agonist) significantly inhibited TSLP, up-regulated occludin, and restored E-cadherin. siGPER and TEER assays suggested that GPER was pivotal for the flavonoids on the epithelial barrier integrity. Finally, G1 attenuated allergic lung inflammation, which could be abolished by G15. Our data demonstrated that 2 flavonoids in Radix Astragali could alleviate allergic asthma by protecting epithelial integrity via regulating GPER, and activating GPER might be a possible therapeutic strategy against allergic inflammation.

Astragaloside IV ameliorates allergic inflammation by inhibiting key initiating factors in the initial stage of sensitization.

To illuminate the anti-allergy mechanism of astragaloside IV (AS-IV), we assessed its effects in a murine model of allergic contact dermatitis (ACD). AS-IV administered in the sensitization phase, rather than in the elicitation phase, dramatically alleviated the symptoms of allergic inflammation. We hypothesized that AS-IV exerts its anti-allergy effects by regulating the production of key pro-allergic cytokines based on the fact that interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) levels increase significantly in the initial stage of the sensitization phase. AS-IV administered in the initial stage of ACD inhibited TSLP and IL-33 expression and reduced the proportion of type-2 innate lymphoid cells (ILC2s). An in vitro study showed that the production of pro-allergic cytokines was significantly inhibited in AS-IV presenting HaCaT cells. We also verified that AS-IV administered only in the initial stage markedly alleviated inflammation, including ear swelling, Th2 cytokine expression, and histological changes. Taken together, these results suggest that AS-IV effectively ameliorates the progression of allergic inflammation by inhibiting key initiating factors, including TSLP and IL-33, and can be used to prevent and/or treat patients with ACD. Our data also suggest that these key pro-allergic cytokines are potential therapeutic targets for allergic diseases.

Therapeutic and recurrence-preventing effects of Qi-Replenishing and Blood-Activating Formula in rats with acetic acid-induced gastric ulcer.

OBJECTIVE: To explore the therapeutic and recurrence-preventing effects of Qi-Replenishing and Blood-Activating Formula in rats with acetic acid-induced gastric ulcer. METHODS: A total of 138 SD rats were selected to make rat models with gastric ulcer induced by acetic acid (24 rats with sham operation served as sham operation group), and were randomly divided into model group (n = 30), western medicine group (n = 30), traditional Chinese medicine (TCM) group (n = 24) and combination group (combined western medicine and TCM group, n = 30). Western medicine group was gavaged with omeprazole in the morning and with iso-volumetric distilled water in the afternoon; TCM group and TCM sham operation group were gavaged with iso-volumetric distilled water in the morning and with Qi-Replenishing and Blood-Activating Formula in the afternoon; combination group was gavaged with omeprazole in the morning and with Qi-Replenishing and Blood-Activating Formula in the afternoon; sham operation group and model group were gavaged with iso-volumetric distilled water both in the morning and afternoon. Ulcer indexes and degree of mucosal degree in rats at different time points after gavage were observed. Twenty-eight days after gavage, interleukin (IL)-1ß was given to induce ulcer recurrence so as to observe the recurrent severity and rate of ulcer in each group. RESULTS: Compared with model group and western medicine group, treatment in combination group could prominently reduce the ulcer index of rats with peptic ulcer, and increase the healing rate and inhibition rate of peptic ulcer. After IL-1ß-induced ulcer recurrence, combination group was significantly superior to model group and western medicine group in ulcer recurrent rate [50% (3/6) vs. 100% (6/6)] and severity. CONCLUSIONS: Basic acid-suppression therapy combined with Qi-Replenishing and Blood-Activating Formula can effectually improve the ulcer healing quality and reduce ulcer recurrence.

[The protection of yupingfeng powder on cisplatin induced oxidative damage of organs in hepatocellular carcinoma mice].

OBJECTIVE: To study the effects of Yupingfeng Powder (YPFP) on cisplatin (DDP) induced oxidative damage of organs in hepatocellular carcinoma mice. METHODS: A total of 2 x10(6) Hepa1 -6 cells were inoculated subcutaneously into the right flank of 15 C57BL/6 mice to establish a mice model of hepatocellular carcinoma. Then the mice were randomly divided into three groups, i.e., the model group, the DDP group, and the DDP + YPFP group, 5 in each group. Mice in the DDP group and the DDP + YPFP group were intraperitoneally injected with DDP (2. 5 mg/kg), once every three day for 2 weeks. Physiological saline was intraperitoneally injected to mice in the model group. Meanwhile, YPFP water decoction (25 g/kg) was given to mice in the DDP + YPFP group by gastrogavage once daily for 2 weeks. Corresponding distilled water was given by gastrogavage to mice in the DDP group and the model group. Fourteen days later, mice were sacrificed and the tumor inhibition ratio was calculated. The weights of kidneys, livers, and lungs were weighed and the organ coefficient calculated. The activities of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the tissue were detected. The pathologic changes were observed. RESULTS: The tumor weight obviously decreased in the DDP group and the DDP + YPFP group when compared with the model group (P < 0.05, P < 0.01). Obvious oxidative damage existed in the kidneys and livers after induced by DDP. Oxidative damage also existed in the lungs to some extent. YPFP could obviously decrease the content of MDA and the activities of SOD in livers (P < 0.05), and increase the activities of SOD in lungs (P < 0.01). The pathologic changes showed the same effect trend. CONCLUSIONS: YPFP could protect the organs (kidney, liver, lung) from the oxidative damage induced by DDP. Anti-oxidation is one of its mechanisms.