Heinoh2086

Osteoarthritis (OA) is a common joint disease and the main cause of disability. We sought to determine the effective concentration of emodin on chondrocytes and to identify the dosage of emodin that induces a comparable therapeutic effect with the COX-2 inhibitor drug, celecoxib that is currently used to treat OA.

In vitro experiments induced inflammation of chondrocytes by IL-1β, and an osteoarthritis model was established in vivo by cutting rat anterior cruciate ligament. Western Blot, Real-time PCR, HE staining, Safranin O-green staining and immunohistochemistry were performed to detect MMP-3, MMP-13, ADAMTS-4, iNOS and COL2A1 on the chondrocytes or the tibial plateau. The cytokine activity and content in serum of six groups of rats were measured by kit.

It was found that the surface layer of the cartilage was thicker and smoother after the administration of emodin. Tissue expression of MMP-3, MMP-13, ADAMTS-4 and iNOS were significantly (p<0.05) decreased in chondrocytes and cartilage treated with different doses of emodin, and the content of COL2A1 was reversed. Emodin also significantly decreased the blood levels of COX-2 and PGE2. The effective emodin in vitro was 5μmol/L, whereas emodin at 80mg/kg was equivalent to celecoxib in vivo.

Emodin reduces the expression of cartilage matrix degradation biomarkers, thereby reducing the degradation of cartilage matrix and protecting the knee joint cartilage. Emodin at 5μmol/L shows the best concentration to treat chondrocytes, and the protective effect of emodin at 80mg/kg is comparable to that of celecoxib.

Emodin reduces the expression of cartilage matrix degradation biomarkers, thereby reducing the degradation of cartilage matrix and protecting the knee joint cartilage. Emodin at 5 μmol/L shows the best concentration to treat chondrocytes, and the protective effect of emodin at 80 mg/kg is comparable to that of celecoxib.Cancer still remains as one of the leading causes of death worldwide. Metastasis and proliferation are abnormally increased in cancer cells that subsequently, mediate resistance of cancer cells to different therapies such as radio-, chemo- and immune-therapy. MicroRNAs (miRNAs) are endogenous short non-coding RNAs that can regulate expression of target genes at post-transcriptional level and capable of interaction with mRNA-coding genes. Vital biological mechanisms including apoptosis, migration and differentiation are modulated by these small molecules. MiRNAs are key players in regulating cancer proliferation and metastasis as well as cancer therapy response. MiRNAs can function as both tumor-suppressing and tumor-promoting factors. In the present review, regulatory impact of miRNA-338-3p on cancer growth and migration is discussed. This new emerging miRNA can regulate response of cancer cells to chemotherapy and radiotherapy. It seems that miRNA-338-3p has dual role in cancer chemotherapy, acting as tumor-promoting or tumor-suppressor factor. Experiments reveal anti-tumor activity of miRNA-338-3p in cancer. Hence, increasing miRNA-338-3p expression is of importance in effective cancer therapy. read more Long non-coding RNAs, circular RNAs and hypoxia are potential upstream mediators of miRNA-338-3p in cancer. Anti-tumor agents including baicalin and arbutin can promote expression of miRNA-338-3p in suppressing cancer progression. These topics are discussed to shed some light on function of miRNA-338-3p in cancer cells.Cancer is accounted as the second-highest cause of morbidity and mortality throughout the world. Numerous preclinical and clinical investigations have consistently highlighted the role of natural polyphenolic compounds against various cancers. A plethora of potential bioactive polyphenolic molecules, primarily flavonoids, phenolic acids, lignans and stilbenes, have been explored from the natural sources for their chemopreventive and chemoprotective activities. Moreover, combinations of these polyphenols with current chemotherapeutic agents have also demonstrated their strong role against both progression and resistance of malignancies. Signal transducer and activator of transcription 3 (STAT3) is a ubiquitously-expressed signaling molecule in almost all body cells. Thousands of literatures have revealed that STAT3 plays significant roles in promoting the cellular proliferation, differentiation, cell cycle progression, metastasis, angiogenesis and immunosuppression as well as chemoresistance through the regulation of its downstream target genes such as Bcl-2, Bcl-xL, cyclin D1, c-Myc and survivin. For its key role in cancer development, researchers considered STAT3 as a major target for cancer therapy that mainly focuses on abrogating the expression (activation or phosphorylation) of STAT3 in tumor cells both directly and indirectly. Polyphenolic molecules have explicated their protective actions in malignant cells via targeting STAT3 both in vitro and in vivo. In this article, we reviewed how polyphenolic compounds as well as their combinations with other chemotherapeutic drugs inhibit cancer cells by targeting STAT3 signaling pathway.Metastasis is one of the leading causes of mortality in cancer patients. As the firstly identified metastasis suppressor, NM23-H1 has been endowed with expectation as a potent target in metastatic cancer therapy during the past decades. However, many challenges impede its clinical use. Accumulating evidence shows that NM23-H1 has a dichotomous role in tumor metastasis as a suppressor and promoter. It has potentially attributed to its versatile biochemical characteristics such as nucleoside diphosphate kinase (NDPK) activity, histidine kinase activity (HPK), exonuclease activity, and protein scaffold, which further augment the complexity and uncertainty of its physiological function. Simultaneously, tumor cells have evolved multiple ways to regulate the expression and function of NM23-H1 during tumorigenesis and metastasis. This review summarized and discussed the regulatory mechanisms of NM23-H1 in cancer including transcriptional activation, subcellular location, enzymatic activity, and protein degradation, which significantly modulate its anti-metastatic function.