Modulating ROS to overcome multidrug resistance in cancer.

The accelerating and thorough treatment of chronic wounds still represents a major unmet medical need owing to the complex symptoms resulting from metabolic disorder of the wound microenvironment. Although numerous strategies and bioactive hydrogels are developed, an effective and widely used method of chronic wound treatment remains a bottleneck. With the aim to accelerate chronic wound healing, many hydrogel dressings with antioxidant functions have emerged and are proven to accelerate wound healing, especially for chronic wound repair. The new strategy in chronic wound treatment brought by antioxidant hydrogels is of great significance to human health. Here, the application of antioxidant hydrogels in the repair of chronic wounds is discussed systematically, aiming to provide an important theoretical reference for the further breakthrough of chronic wound healing.

Advances and Impact of Antioxidant Hydrogel in Chronic Wound Healing.

Cutaneous wound healing is the process by which skin repairs itself. It is generally accepted that cutaneous wound healing can be divided into 4 phases: haemostasis, inflammation, proliferation, and remodelling. In humans, keratinocytes re-form a functional epidermis (reepithelialization) as rapidly as possible, closing the wound and reestablishing tissue homeostasis. Dermal fibroblasts migrate into the wound bed and proliferate, creating “granulation tissue” rich in extracellular matrix proteins and supporting the growth of new blood vessels. Ultimately, this is remodelled over an extended period, returning the injured tissue to a state similar to that before injury. Dysregulation in any phase of the wound healing cascade delays healing and may result in various skin pathologies, including nonhealing, or chronic ulceration. Indigenous and traditional medicines make extensive use of natural products and derivatives of natural products and provide more than half of all medicines consumed today throughout the world. Recognising the important role traditional medicine continues to play, we have undertaken an extensive survey of literature reporting the use of medical plants and plant-based products for cutaneous wounds. We describe the active ingredients, bioactivities, clinical uses, formulations, methods of preparation, and clinical value of 36 medical plant species. Several species stand out, including Centella asiatica, Curcuma longa, and Paeonia suffruticosa, which are popular wound healing products used by several cultures and ethnic groups. The popularity and evidence of continued use clearly indicates that there are still lessons to be learned from traditional practices. Hidden in the myriad of natural products and derivatives from natural products are undescribed reagents, unexplored combinations, and adjunct compounds that could have a place in the contemporary therapeutic inventory.

/pdf/wound-healing-and-the-use-of-medicinal-plants-5c63kejquu.pdf

Wound healing and the use of medicinal plants

Antioxidant hydrogel has exhibited great potential for diabetic wound treatment. However, it is still a difficult challenge to realize reactive oxygen species (ROS) scavenging in an intelligent manner. Herein, we designed a novel glucose-responsive antioxidant hybrid hydrogel for enhanced diabetic wound repair. In this study, phenylboronic acid (PBA) with unique glucose-sensitivity was modified onto a hyaluronic acid (HA) chain by one-step synthesis, which was then incorporated into a polyethylene glycol diacrylates (PEG-DA) hydrogel matrix to obtain a novel hybrid hydrogel (PEG-DA/HA-PBA). Then, myricetin (MY) molecules with strong antioxidant activity were immobilized into the hybrid hydrogel by the formation of a dynamic borate bond between the polyphenol group of MY and the phenylboronic acid group of HA-PBA. The PEG-DA/HA-PBA/MY (PHM) hybrid hydrogel achieved glucose-triggered MY release, efficient ROS-scavenging (>80.0%), and also reshaped the hostile oxidative wound microenvironment (reduced MDA activity and increased SOD and GSH/GSSG levels). Furthermore, in vitro and in vivo results indicated that the PHM hydrogel platform effectively ameliorated the inflammatory response (decreased IL-6 and increased Il-10 expression), accelerated angiogenesis (increased VEGF and CD 31 expression), and increased tissue remodeling within 20 days, which was better than the nonresponsive PEG-DA/MY (PM) hydrogel platform in promoting diabetic wound healing. All results strongly suggested that this novel glucose-responsive antioxidant hybrid hydrogel platform has great potential in diabetic wound repair.

Novel Glucose-Responsive Antioxidant Hybrid Hydrogel for Enhanced Diabetic Wound Repair.

Shikonin derivatives for cancer prevention and therapy

Shikonin inhibits gefitinib-resistant non-small cell lung cancer by inhibiting TrxR and activating the EGFR proteasomal degradation pathway.

EGFR and KRAS mutations are the two most common driver mutations in non-small cell lung cancer (NSCLC). Molecular target-based therapy using small molecules such as gefitinib has been used for inhibiting EGFR with good initial responses; however, drug resistance is common when using a mono-targeting strategy. At present, KRAS remains an undruggable target. As such, the development of new drugs targeting the downstream of KRAS and EGFR and their crosstalk pathways is critically needed to effectively treat NSCLC. The present study aimed to elucidate the anticancer effects of PI3K (BKM120) and MEK (PD1056309) inhibitors on NSCLC cell lines with KRAS or EGFR mutations. Inhibition of the EGFR and KRAS downstream P13K pathway using BKM120 significantly inhibited the growth of NSCLC cell lines with either EGFR or KRAS mutations. In addition, significant cell cycle arrest and induction of apoptosis were observed following BKM120 treatment. Notably, although the A549 and H358 NSCLC cell lines harbor the same KRAS mutation, A549 cells were less sensitive than H358 cells in the response to BKM120 treatment. Similarly, PC-9 and H1650 cells harbor the same EGFR mutation, however, H1650 was less sensitive to BKM120. Different sensitivity between NSCLC cell lines with the same oncogenic mutation suggests that multiple crosstalk pathways exit. Combined usage of BKM120 and PD1056309 synergistically enhanced apoptosis in the A549 cells and mildly enhanced apoptosis in the H1650 and H358 cells, suggesting the crosstalk of the MEK pathway with the P13K/Akt pathways in these cell lines. Overall, our findings suggest that inhibition of EGFR and KRAS downstream with a P13K/Akt inhibitor could be useful for treating NSCLC. However, for NSCLC exhibiting crosstalk with other survival pathways, such as the MEK pathway, combination treatment is required.

/pdf/combined-use-of-pi3k-and-mek-inhibitors-synergistically-z8brd6r9jl.pdf

Combined use of PI3K and MEK inhibitors synergistically inhibits lung cancer with EGFR and KRAS mutations.

The present invention provides a compound suitable for treating EGFR-dependent non-small cell lung cancer, which exceptionally inhibits activity of the EGFR kinase, in particular in EGFR-dependent non-small cell lung cancer with intrinsic or acquired resistance against at 5 least one EGFR inhibitor. Further, methods for inhibiting EGFR kinase activity in non-small cell lung cancer cells which harbor an abnormality in the EGFR gene and for targeting cancer cells harboring an abnormality in EGFR gene by contacting EGFR-dependent non small cell lung cancer cells with said compound are provided. The compound of the invention allows for an advantageous inhibition of the EGFR kinase 0 activity and induction of apoptosis of the non-small cell lung cancer cells with abnormality in the EGFR gene. Hence, said compound represents a highly promising treatment option for patients harboring EGFR-dependent cancer.

Hydroxynaphthoquinone compounds for treatment of non-small cell lung cancer

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Shikonin inhibits gefitinib-resistant non-small cell lung cancer by inhibiting TrxR and activating the EGFR proteasomal degradation pathway.

Combined use of PI3K and MEK inhibitors synergistically inhibits lung cancer with EGFR and KRAS mutations.

Hydroxynaphthoquinone compounds for treatment of non-small cell lung cancer