A Clinical Observation and Study on Prunella Vulgaris Decoction in Promoting the Repair of Chronic Infective Refractory Wounds

Objective: To further study the clinical efficacy of prunella vulgaris decoction in promoting the repair of chronic infective refractory wounds, and analyze and evaluate the feasibility of this treatment. Methods: A total of 80 patients with chronic infective refractory wounds were screened out from a hospital from March 2020 to March 2021. The random sampling method was used to divide the patients into the experimental group and reference group. The experimental group was treated with prunella vulgaris decoction while the reference group was treated with routine wound dressing change. Wound repair rate, bacterial negative conversion rate, healing time and clinical comprehensive efficacy in the two groups were used as evaluation indexes in this study. Results: After different treatment, the conditions of the patients in the two groups were statistically analyzed. It was found that the wound repair rate, bacterial negative conversion rate and total effective rate of the experimental group were much higher than that of the reference group. In addition, the wound healing time in the experimental group was also significantly shortened compared with that of the reference group. Conclusion: Prunella vulgaris decoction bears obvious anti-inflammatory and anti-bacterial effects and can accelerate the speed of wound repair, which has great practical value in clinic treatment and prosperous prospect in future development and application

Study on the Bacteriostatic Effect of Baitouweng on Pseudomonas Aeruginosa Infection of Wounds in Rats

Objective: To analyze the bacteriostatic effect of Baitouweng on Pseudomonas aeruginosa infection of wounds in rats. Methods: Forty Wistar rats were enrolled in the study, among which excisions were made on 30 rats on their upper layer of dorsal skin with an area of 1 cm x 1 cm, the other 10 rats as the control group of sterile wound. Prepared Pseudomonas aeruginosa was applied on the wounds of rats to create infection models. Forty rats were divided into three groups (control group, mafenide group and Baitouweng group) according to different infection methods, and were treated with normal saline, 100g/L mafenide, and 1g/L Baitouweng respectively after 3 hours of injury. The changes in the number of white blood cells in both the wound surface and body of the three groups were observed within one to four days after injury. After that, the changes on the number of both white blood cells and body weight were continuously observed. The survival of the rats in each group was observed on the 14th day after injury. Results: From the observation after injury, compared with the other two groups, rats in control group had more exudation and moist wounds, and the activities of rats decreased while the death rate increased. On the 3rd day after injury, the number of white blood cells in each group decreased, and the number of Pseudomonas aeruginosa in the control group was significantly higher than that in the other two groups (P < 0.01). The rats in the sterile wound control group did not die and continued to gain weight. After 14 days, the survival number of rats in control group was significantly less than that in mafenide group and Baitouweng group (P<0.05). Conclusion: Baitouweng has obvious bacteriostatic and virus-killing effects on Pseudomonas aeruginosa infection of wounds in Wistar rats, reducing mortality rate effectively, and has practical value as well as development and application prospects

31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016) : part two

Background The immunological escape of tumors represents one of the main ob- stacles to the treatment of malignancies. The blockade of PD-1 or CTLA-4 receptors represented a milestone in the history of immunotherapy. However, immune checkpoint inhibitors seem to be effective in specific cohorts of patients. It has been proposed that their efficacy relies on the presence of an immunological response. Thus, we hypothesized that disruption of the PD-L1/PD-1 axis would synergize with our oncolytic vaccine platform PeptiCRAd. Methods We used murine B16OVA in vivo tumor models and flow cytometry analysis to investigate the immunological background. Results First, we found that high-burden B16OVA tumors were refractory to combination immunotherapy. However, with a more aggressive schedule, tumors with a lower burden were more susceptible to the combination of PeptiCRAd and PD-L1 blockade. The therapy signifi- cantly increased the median survival of mice (Fig. 7). Interestingly, the reduced growth of contralaterally injected B16F10 cells sug- gested the presence of a long lasting immunological memory also against non-targeted antigens. Concerning the functional state of tumor infiltrating lymphocytes (TILs), we found that all the immune therapies would enhance the percentage of activated (PD-1pos TIM- 3neg) T lymphocytes and reduce the amount of exhausted (PD-1pos TIM-3pos) cells compared to placebo. As expected, we found that PeptiCRAd monotherapy could increase the number of antigen spe- cific CD8+ T cells compared to other treatments. However, only the combination with PD-L1 blockade could significantly increase the ra- tio between activated and exhausted pentamer positive cells (p= 0.0058), suggesting that by disrupting the PD-1/PD-L1 axis we could decrease the amount of dysfunctional antigen specific T cells. We ob- served that the anatomical location deeply influenced the state of CD4+ and CD8+ T lymphocytes. In fact, TIM-3 expression was in- creased by 2 fold on TILs compared to splenic and lymphoid T cells. In the CD8+ compartment, the expression of PD-1 on the surface seemed to be restricted to the tumor micro-environment, while CD4 + T cells had a high expression of PD-1 also in lymphoid organs. Interestingly, we found that the levels of PD-1 were significantly higher on CD8+ T cells than on CD4+ T cells into the tumor micro- environment (p < 0.0001). Conclusions In conclusion, we demonstrated that the efficacy of immune check- point inhibitors might be strongly enhanced by their combination with cancer vaccines. PeptiCRAd was able to increase the number of antigen-specific T cells and PD-L1 blockade prevented their exhaus- tion, resulting in long-lasting immunological memory and increased median survival

The protective effects of bexarotene against advanced glycation end-product (AGE)-induced degradation of articular extracellular matrix (ECM)

AbstractOsteoarthritis (OA) is a common debilitating disease primarily characterised by excessive loss of the articular ECM, which is composed of up to 95% type II collagen. Among the factors that contribute to the pathogenesis of OA, the natural process of aging is regarded as the most significant risk factor. AGEs, which are extremely resilient to degradation, are produced in the body naturally as a result of the Maillard process of nonenzymatic glycation and are also introduced through diet and tobacco smoke. AGEs have a high affinity for collagen and therefore accumulate in joint tissues, where they induce increased expression of proinflammatory cytokines, chemokines, and degradative enzymes. Additionally, AGEs induce oxidative stress, which further exacerbates the degradative process. Type II collagen is targeted for degradation by matrix metalloproteinases (MMPs), particularly MMP-3 and MMP-13, and AGEs have been shown to trigger increased expression of these MMPs. The role of retinoid and rexinoid receptors as specific treatment targets has been receiving increasing attention. Bexarotene is a retinoid X receptor (RXR) agonist used for the treatment of T-cell lymphoma and other cancers which has displayed a favourable safety profile. Here, we examined the roles of RXR agonism using bexarotene on AGE-induced markers of OA, including oxidative stress, inflammatory response, and MMP-mediated degradation of type II collagen. Furthermore, we demonstrate that bexarotene inhibited phosphorylation of IκBα, thereby suppressing activation of the proinflammatory NF-κB cellular signalling pathway. These findings present a basis for selective targeting of RXR by bexarotene as a potential treatment of OA induced by AGEs