Zvast Biotechnology
Skin Laceration
The pig skin laceration model is a SCI gold-standard large-animal skin soft tissue trauma repair model constructed by standardized mechanical force, which accurately simulates the whole process of full-thickness skin laceration injury and natural wound healing caused by clinical external force tearing, falling and mechanical friction, and completely compensates for the research shortcomings of rodent small animals such as mice and rats with great differences in skin structure and healing mechanism from humans. Porcine skin tissue structure, epidermal and dermal layer thickness, collagen fiber arrangement, skin blood perfusion, epidermal regeneration cycle and post-traumatic inflammatory repair mechanism are highly homologous to humans. Skin tension, toughness, ductility and post-injury scar hyperplasia rules are completely consistent with clinical human skin trauma characteristics, making it the non-human mammalian skin trauma large-animal model with the highest clinical transformation value. Standardized controllable mechanical tearing is adopted to accurately destroy the entire epidermis and dermis of the dorsal skin of experimental pigs and superficial subcutaneous connective tissue, constructing acute skin laceration wounds with regular boundaries, uniform damage and controllable bleeding volume. After trauma, the body rapidly initiates acute inflammatory response, activates core repair pathways such as NF-κB, TGF-β/Smad and PI3K/Akt, and sequentially undergoes inflammatory exudation, inflammatory cell infiltration, granulation tissue neogenesis, collagen deposition, epidermal re-epithelialization and wound contraction and remodeling, which fully recapitulates the pathophysiological process of natural healing of human acute skin laceration trauma-inflammation activation-granulation proliferation-scar remodeling. With controllable injury degree, high wound uniformity, stable healing cycle and minimal individual differences, and no interference of spontaneous infection and abnormal healing, this model serves as an authoritative SCI gold-standard large-animal model for the elucidation of skin trauma repair mechanisms, preclinical evaluation of new anti-inflammation and regeneration-promoting drugs, collagen remodeling regulation, anti-scar hyperplasia drugs and medical dressings.
The skin of the blank group was intact and smooth with uniform color and no swelling or exudation. Immediately after operation, the model group formed full-thickness skin lacerations with clear boundaries and uniform depth, irregular wound edges and a small amount of bloody exudate, without large-area subcutaneous hematoma and skin necrosis and shedding. The wounds showed obvious swelling and increased inflammatory exudation on Day 3 after operation; granulation tissue neogenesis and wound contraction and narrowing were observed on Day 7; epidermis gradually crawled and covered the wounds with scab formation and shedding from Day 14 to Day 21, presenting typical temporal characteristics of trauma healing including inflammatory exudation-granulation proliferation-epidermal regeneration-wound remodeling, with stable wound healing rate and minimal intra-group differences, confirming preliminary successful model construction.
Image analysis software was used to accurately measure wound area at each time point and calculate wound healing rate. The wounds of the model group decreased regularly over time after operation, with stable healing rate gradient at each time point and consistent with the kinetic law of normal skin trauma repair. There was a significant difference from the intact skin of the blank group, and the dispersion of wound healing data within the group was extremely low, with no individuals with delayed healing, abnormal proliferation, infection and ulceration, serving as the core quantitative gold standard index for successful modeling.
HE and Masson staining of skin tissues showed typical pathological evolution of laceration repair: 3 days after operation, the continuity of epidermis and dermis was interrupted, with massive infiltration of neutrophils, macrophages and lymphocytes and obvious tissue edema; 7 days after operation, the wounds were rich in neonatal granulation tissue with massive proliferation of fibroblasts and dense distribution of neonatal microvessels and loosely arranged collagen fibers; 14–21 days after operation, collagen fibers were orderly deposited, epidermal re-epithelialization was completed, and skin tissue structure was gradually remodeled and repaired, which fully recapitulates the pathological repair process of acute inflammation-granulation proliferation-collagen remodeling of human skin lacerations with typical and highly specific pathological phenotypes.
In the acute stage of model group wound tissues, pro-inflammatory factors TNF-α, IL-6 and IL-1β were significantly highly expressed with obvious inflammatory pathway activation; in the repair stage, the expression of repair-promoting factors VEGF, TGF-β and bFGF was significantly upregulated, with enhanced fibroblast activation, angiogenesis and collagen synthesis capacity, which fully conforms to the core mechanism of inflammatory response and regenerative repair of skin lacerations and serves as the core academic basis for successful model construction.
As a SCI-certified exclusive large-animal gold-standard repair model for skin lacerations, it completely breaks through the species defects of rodent small animals such as excessive fast skin healing, contraction-dominated healing and no human epidermal regeneration characteristics. Porcine skin structure, traumatic response, collagen remodeling and scar formation mechanism are highly consistent with humans, and the healing mode is re-epithelialization repair, which fully conforms to the healing law of human clinical skin lacerations. The modeling method adopts precisely controllable mechanical external force with unified wound specifications, uniform damage, no mixed drug intervention factors, pure mechanism and excellent reproducibility. It has moderate modeling cost, extremely low postoperative mortality and clear healing cycle gradient, which can completely distinguish repair differences in inflammatory stage, proliferation stage and remodeling stage. It is specially suitable for large-animal preclinical evaluation of anti-inflammatory, granulation regeneration-promoting, epidermal repair-promoting, ordered collagen deposition-regulating and scar hyperplasia-inhibiting drugs and medical dressings. With clear project mechanism, extremely high translational value and high recognition in high-score SCI journals, it is fully applicable for fund declaration, project opening, master and doctoral theses and translational medical research of skin trauma repair.
The pig skin laceration model is corely applied to basic research on inflammatory response mechanism of acute skin mechanical trauma, fibroblast proliferation and granulation tissue regeneration, angiogenesis regulation, collagen deposition and skin remodeling, and epidermal re-epithelialization repair. It is specially used for screening and evaluating traditional Chinese medicine compounds, natural active ingredients, small chemical molecules, wound repair preparations and medical dressings with effects of anti-inflammation and detumescence, promoting wound granulation growth, accelerating epidermal regeneration, optimizing collagen remodeling and inhibiting scar hyperplasia. It is widely used in the exploration of skin trauma repair targets, elucidation of wound regeneration mechanisms and large-animal preclinical translational verification of trauma repair drugs and medical consumables, serving as an indispensable standardized large-animal gold-standard model in the fields of skin surgery, trauma repair, regenerative medicine and anti-scar research.
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