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Background This study aimed to investigate the mechanism of action of Panax notoginoside (PNS) against lung cancer and inhibition of lung cancer cell proliferation by the drug at different concentrations in a mouse model, considering the cathepsin B (CTSB) gene as a target. Methods The mice were randomly assigned into the following five groups: normal control, tumor-bearing, low-dose Panax notoginoside (TSPN), medium-dose TSPN, and high-dose TSPN. All mice were treated with physiological saline or TSPN at different concentrations for 28 days consecutively by gavage. The tumor size was measured, the tumor growth was observed, and the survival curve was drawn. At different time points, the expression of the CTSB gene was detected using quantitative fluorescent polymerase chain reaction, Western blot analysis, and indirect immunofluorescence. The serum indices, such as carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), and Soluble fragment of cytokeratin 19 (CYFRA21), were detected by enzyme-linked immunosorbent assay. Results In vivo, PNS could directly inhibit the expression of the CTSB gene in tumors of mice, limit tumor growth, and alter tumor-related indices, such as CEA, NSE, and CYFRA21 levels, in the serum to different extents simultaneously. Conclusion CTSB gene was closely related to the pathogenesis of lung cancer. PNS could act on the CTSB gene, downregulate the expression of CTSB in lung cancer cells, inhibit the proliferation and invasion of tumors, and prolong the survival period.

Panax notoginseng saponin (PNS) constitutes the major effective components of Panax notoginseng, which is widely used to treat microcirculatory disturbance associated diseases. In this study, we designed to investigate the effect of PNS on the treatment of pulmonary fibrosis (PF) and further explored its mechanism. A total of 40 healthy Japanese White rabbits were randomly divided into five groups (control group; PF model group; PNS prevention group; PNS treatment group; and western medicine [prednisone acetate] treatment group). Expression of hydroxyproline (HYP), fibronectin (FN), aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), interleukin-6 (IL-6), and interleukin-8 (IL-8) in serum was detected using corresponding detection kits. Western blot was applied to detect the expression of p50 and p65 in pulmonary tissues. The pathological variations of the cardiac and pulmonary ultrastructure were observed under both the optical and electron microscope. PF models were established successfully. The results showed that compared with the other groups, PNS groups (PNS prevention and treatment group) apparently relieved the cardiopulmonary injury, and reduced IL-6 and IL-8 expression levels in the serum. Furthermore, the PNS groups performed better in relieving cardiopulmonary injurythan other groups. Both the PNS groups and the western medicine treatment group presented an obvious role in relieving PF. We concluded that PNS could reduce the expression of AST, LDH, CK, IL-6, and IL-8 in serum of the rabbits, relieve the pathological ultrastructure of cardiopulmonary injury, alleviate PF. And it might be attributed to the inhibition on the NF-κB signaling pathway.

Royal jelly (RJ) possesses biological effects on varied organisms. The objective of this study was to investigate the effect of RJ on tumour growth with transcriptomic profile. RJ intake for 42 days did inhibit tumour growth in 4T1-bearing mice, and gene expression profile of tumour was determined by high-throughput RNA sequencing system. Out of 281 differently expressed genes (DEGs), 56 were annotated with immune system processes, suggesting that RJ immunomodulation was response to the tumour growth in 4T1-bearing mice. KEGG pathway analysis had shown that only four pathways were notably enriched in tumour of RJ-treated 4T1-bearing mice. DEG ratios related to immunity in these four pathways were very high. Overlapping DEGs of these four pathways were all related to immunity. These findings showed that tumour growth in 4T1-bearing mice was affected by RJ-induced alterations in gene expression and related pathways, especially the immune-related genes.

Background Skin injury is inevitable in daily life. In recent years, with the increasing morbidity of diseases such as diabetes and metabolic disorders, chronic wounds have become a considerable challenge in clinical practice. Royal jelly, reported to have multifarious biological and physiological properties, has been used as a remedy for a variety of wounds since ancient times. However, the active components and mechanisms underlying the wound-healing properties of royal jelly are still largely unknown. Methods Water-soluble proteins of royal jelly were fractionated and investigated for the proliferative and migratory effects on human epidermal keratinocytes (HaCaT) in an in vitro wound healing model. The proteins present in bioactive fractions were characterised and quantified using Label-free protein quantification method. The potential functions of these proteins in biological systems were further analysed using bioinformatic tools. Results A protein fraction, mainly containing major royal jelly proteins 2 (MRJP2), MRJP3 and MRJP7, stimulated proliferative and migratory activities in HaCaT cells without visible cytotoxicity. It exerted the greatest effects on the growth of HaCaT cells in the first 48 h. Furthermore, when treated with this protein fraction, the closure rates of the in vitro scratch wound were significantly increased. Functional analysis indicated that MRJP2, MRJP3 and MRJP7 were associated with carbohydrate transport and metabolism. Conclusions We fractionated the water-soluble proteins of royal jelly and identified one fraction (Fraction 2) that induced both proliferative and migratory effects on a human epidermal keratinocyte cell line. Major royal jelly proteins (MRJP2, MRJP3 and/or MRJP7) were speculated to possess potential wound-healing bioactivity. This is the first report that royal jelly may improve wound closure via MRJP-induced cellular proliferation and migration. These proteins may be valuable lead compounds for the development of novel wound healing medications. Our findings would facilitate better understanding of the wound repair mechanisms of royal jelly.

Due to various pharmacological properties, including antioxidative, anti-inflammatory and antibiotic properties, royal jelly (RJ) has been widely consumed in daily diets in numerous countries. In the present study, the effect of RJ on 4T1-bearing mice was investigated. The study was performed by feeding 4T1-bearing mice with RJ using either the prophylactic-therapeutic (PTRJ) or therapeutic (TRJ) method. The experimental results for the PTRJ group demonstrated that the weight of tumor was significantly reduced (RJ 0.5 and 1.5 g/kg); and in the serum, the levels of interleukin (IL)-2 (RJ 0.5 and 1.5 g/kg), interferon (IFN)-α, superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) were significantly elevated, but the concentrations of IL-4 (RJ 0.5 and 1.5 g/kg) and IL-10 (RJ 1.0 g/kg) were significantly decreased. In addition, the activities of T-AOC and glutathione reductase (GR) were significantly improved in the liver, whereas in the kidney, the activities of T-AOC and GR were significantly increased only under the dose of 0.5 g/kg. For the TRJ group, the antitumor effect of RJ was not significant; the change in IL-2, IFN-α, SOD and T-AOC levels in the serum, and the change in T-AOC and GR in liver were similar to those observed in the PTRJ groups. RJ treatment was demonstrated to reduce the development of breast tumor in mice, and simultaneously improve the antioxidant capacity of the serum, liver and kidney, particularly using the prophylactic-therapeutic method. These results corroborated the efficacy of RJ supplementation in diets. The results of the present study suggest that the antioxidant and immunomodulatory activities of RJ serve an important role on antitumor growth.