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Aplastic anemia, life-threatened disease, is a hematologic disorder characterised by bone marrow hypoplasia. Multiple modalities such as bone marrow transplantation and immunosuppression treatment have been proposed to ameliorate this entity, however it remains ineffective. Sambucus, a group of herb plants, possesses a broad spectrum of medicinal properties such as antioxidant, insulin-like activity, anticancer and antiviral. However, the study about its activity toward aplastic anemia incidence is based on limited data. Thus, the research aim of this study was to evaluate the immunomodulatory activities of Sambucus javanica in chloramphenicol-induced anemia aplastic mouse model. In this present study, BALB/c mice were administrated with chloramphenicol (CMP) to induce aplastic anemia then followed by S. javanica extracts treatment. Additionally, cellular and molecular aspects were evaluated by flow cytometry and Hematoxylin-Eosin staining. Further analysis showed that S. javanica extracts could promote the population number of regulatory T-cells and naive cytotoxic T-cells. Moreover, those extract also reduced the inflammation and necrotic incidence in CMP-induced mouse aplastic anemia model. Together, these results suggest that S. javanica has therapeutically effect to aplastic anemia by altering the immune system as an immunomodulatory agent.

Liver fibrosis is the initial step of hepatocellular carcinoma (HCC). Liver fibrosis can be triggered by metabolic perturbation, viral infection, and harmful chemical exposure. This in vivo study aims to investigate the potential of Moringa oleifera leaf powder (MOLP) from Madura Island as the future candidate for antifibrosis and hepatoprotective agent. The study was conducted to evaluate the alteration of circulating levels of liver injury marker-linked liver fibrosis development, Alanine Aminotransferase (ALT), and Aspartate Aminotransferase (AST). The animal model was prepared using Balb-c mice age 6-8 weeks treated by intraperitoneal injection of carbon tetrachloride (CCl4) dose 1 µL/g of BW for six weeks to induce liver fibrosis. The experimental groups were received green materials Moringa oleifera leaf powder solution with a serial dosage by peroral administration for six weeks. Interestingly, our animal model's preliminary study shows that the administration of green materials MOLP can alleviate the increase of ALT and AST. MOLP treatment can also prevent significant changes in liver weight, morphology, and even histological feature-associated liver injury and fibrosis. Hence, MOLP Madura Island may become the future green materials source for cancer herbal drug development.

Chronic inflammation is the initial stage of liver fibrosis-related hepatocellular carcinoma (HCC) development. Also, HCC is a global disease resulting from several etiological factors. HCC incidence can be triggered by alcohol abuse, non-alcoholic steatohepatitis (NASH), viral hepatitis B (HBV), viral hepatitis C (HCV), and non-alcoholic fatty liver disease (NAFLD). Liver chronic inflammation significantly correlates to TNF-α (Tumor Necrosis Factor-α) and IL-6 (interleukin 6) expression. This laboratory work aimed to investigate the effect of green material Moringa oleifera leaf powder (MOLP) on the expression of both pro-inflammatory cytokines. A semi-quantitative approach quantified the expression of TNF-α and IL-6. This research was conducted using an animal model induced by intraperitoneal injection of CCl4 solution. The results showed that green material Moringa oleifera could reduce IL-6 and TNF-α expression. Importantly, MOLP exposure can decrease the pro-inflammatory cell population in the liver parenchymal area. Hence, the application of green material Moringa oleifera might be potential as the local bioresources agent against liver inflammation-linked fibrosis. The exploration of MOLP in the future drug discovery model may significantly contribute to the prevention of hepatocellular carcinoma.

The ability of tumor cells to escape immune destruction and their acquired resistance to chemotherapy are major obstacles to effective cancer therapy. Although immune checkpoint therapies such as anti-PD-1 address these issues in part, clinical responses remain limited to a subpopulation of patients. In this report, we identified IL34 produced by cancer cells as a driver of chemoresistance. In particular, we found that IL34 modulated the functions of tumor-associated macrophages to enhance local immunosuppression and to promote the survival of chemoresistant cancer cells by activating AKT signaling. Targeting IL34 in chemoresistant tumors resulted in a remarkable inhibition of tumor growth when accompanied with chemotherapy. Our results define a pathogenic role for IL34 in mediating immunosuppression and chemoresistance and identify it as a tractable target for anticancer therapy. Cancer Res; 76(20); 6030–42. ©2016 AACR.