Polysaccharide-based chondroitin sulfate macromolecule loaded hydrogel/scaffolds in wound healing- A comprehensive review on possibilities, research gaps, and safety assessment.

Wound healing is an intricate multifactorial process that may alter the extent of scarring left by the wound. A substantial portion of the global population is impacted by non-healing wounds, imposing significant financial burdens on the healthcare system. The conventional dosage forms fail to improve the condition, especially in the presence of other morbidities. Thus, there is a pressing requirement for a type of wound dressing that can safeguard the wound site and facilitate skin regeneration, ultimately expediting the healing process. In this context, Chondroitin sulfate (CS), a sulfated glycosaminoglycan material, is capable of hydrating tissues and further promoting the healing. Thus, this comprehensive review article delves into the recent advancement of CS-based hydrogel/scaffolds for wound healing management. The article initially summarizes the various physicochemical characteristics and sources of CS, followed by a brief understanding of the importance of hydrogel and CS in tissue regeneration processes. This is the first instance of such a comprehensive summarization of CS-based hydrogel/scaffolds in wound healing, focusing more on the mechanistic wound healing process, furnishing the recent innovations and toxicity profile. This contemporary review provides a profound acquaintance of strategies for contemporary challenges and future direction in CS-based hydrogel/scaffolds for wound healing.

Crosstalk between ROS-inflammatory gene expression axis in the progression of lung disorders.

A significant number of deaths and disabilities worldwide are brought on by inflammatory lung diseases. Many inflammatory lung disorders, including chronic respiratory emphysema, resistant asthma, resistance to steroids, and coronavirus-infected lung infections, have severe variants for which there are no viable treatments; as a result, new treatment alternatives are needed. Here, we emphasize how oxidative imbalance contributes to the emergence of provocative lung problems that are challenging to treat. Endogenic antioxidant systems are not enough to avert free radical-mediated damage due to the induced overproduction of ROS. Pro-inflammatory mediators are then produced due to intracellular signaling events, which can harm the tissue and worsen the inflammatory response. Overproduction of ROS causes oxidative stress, which causes lung damage and various disease conditions. Invasive microorganisms or hazardous substances that are inhaled repeatedly can cause an excessive amount of ROS to be produced. By starting signal transduction pathways, increased ROS generation during inflammation may cause recurrent DNA damage and apoptosis and activate proto-oncogenes. This review provides information about new targets for conducting research in related domains or target factors to prevent, control, or treat such inflammatory oxidative stress-induced inflammatory lung disorders.