Neurosurgeons Must Be Aware of the Importance of Zinc in Wound Healing


Studies demonstrate the significance of zinc for wound healing. Neurosurgeons must remain up-to-date with scientific data regarding their role in post-neurological wound repair and healing. Look into the Best info about قرص یونی زینک.

Zinc supplementation enhances regulatory T lymphocyte responses that help alleviate inflammation and support epithelialization; this facilitates wound repair.


Zinc is an indispensable metal essential to cell functioning and immune health. Zinc can bind with and modulate many enzymes involved in wound healing such as protein Kinase C (PKC), Cytochrome Oxidase, DNA Ligases, as well as those involved with oxidative stress responses such as DNA Ligases. Zinc also facilitates epithelization while decreasing inflammation as well as bacteria growth.

Clinicians must recognize the signs of zinc deficiency in their patients as it can interfere with or delay wound healing, including an ineffective immune response, poor granulation tissue formation, and reduced cell proliferation.

Zinc is essential in producing inflammatory cells like neutrophils and macrophages, which play a crucial role in inflammation by clearing debris, activating pathways to activate inflammation, secreting various cytokines and growth factors and engaging in phagocytosis and producing nitric oxide which contributes to vasodilation and thrombolysis.

Studies have demonstrated that topical zinc sulfate (ZnSO4) can aid wound reepithelialization while simultaneously decreasing inflammation and bacteria growth, possibly as a result of inducing metallothionein expression in skin tissue and increasing collagen degradation within necrotic tissue necrosis.


Wound healing is an intricate process requiring coordination among various cell types. Zinc plays an essential role in cell membrane repair, growth and differentiation as well as immune regulation and modulation; deficiencies of zinc may disrupt both adaptive immune responses as well as alter innate responses resulting in abnormal inflammation or slow wound closure.

Just after injury, hemostasis begins with activation and aggregation of platelets to form an initial clot to stop bleeding. Zinc plays an essential role here by stimulating platelet activation via protein kinase C-mediated tyrosine phosphorylation of -granule proteins; additionally, it enhances thrombin formation to initiate the coagulation phase of hemostasis.

Zinc can bind to the protease inhibitor MG53 in intracellular vesicles and facilitate its use to cleave off galactosidase from extracellular matrix proteins during tissue remodelling stage of wound healing, helping remove them and release their constituent -galactosidase enzyme. At this point, MG53 also helps control macrophage phagocytosis of ECM proteins while at the same time increasing fibroblast-generated ECM accumulation during this stage.

The inflammatory phase of wound healing is vital in repairing tissue damage; however, excessive inflammation can prevent its proper closure. Monocytes and neutrophils play an integral part in mitigating this inflammation by upregulating inducible nitric oxide synthases (iNOS), producing reactive nitrogen species to kill microbes and limit tissue damage. But excessive reactions may delay wound healing timeframes and chronic infections, increasing Tregs may reduce inflammation to promote wound reepithelization. Zinc can improve Treg numbers to promote wound reepithelization by suppressing inducible niNOS upregulation, thereby producing reactive nitrogen species to kill microbes as iNOS makes reactive nitrogen species to kill microbes while killing microbes with reactive nitrogen species had reactive nitrogen species while killing microbes that kill microbes in order to kill microbes which kill microbes thus creating reactive nitrogen species killing microbes while simultaneously killing microbes thereby killing microbes while killing microbes at once can result in delayed healing time as chronic infections; Zinc may help with increasing regulatory T lymphocytes (Tregs), thus inhibit inflammation while stimulating wound re-epithelization by increasing number of T lymphocytes to counteract inflammation while enabling wound re-epithelization.

Growth Factors

Zinc is an essential trace element to human physiology and plays a critical role in wound healing. As cofactor for several metalloenzymes required for cell membrane repair, growth, and immune function; zinc deficiency leads to skin lesions, growth retardation and compromised wound healing.

As part of its healing process, wound sites must first establish hemostasis by way of coagulation and inflammation to clear debris and infectious microbes away. Next comes granulation tissue formation which is dependent on proliferation of fibroblasts and epithelial cells to deposit extracellular matrix (ECM) that supports tissue remodelling and closure; Zinc is required for these processes as it stimulates their growth as well as collagen development, an essential component of extracellular matrix.

Zinc can assist wound healing during its inflammatory phase by upregulating regulatory T (Treg) lymphocytes that help resolve inflammation and facilitate wound re-epithelization. Furthermore, zinc helps activate and sustain M2 macrophages, which clear pathogens away while simultaneously destroying damaged tissue and suppressing inflammation during later stages.

Recent studies have uncovered the critical roles played by TRIM proteins such as TRIM28 and TRIM16 in mediating inflammation as well as angiogenesis during wound healing. Zinc has been demonstrated to regulate both expression and function of these two TRIMs proteins, suggesting a better understanding of its regulation by Zinc will allow us to optimize therapeutic approaches using regenerative medicine more effectively.


Zinc, an essential micronutrient, plays a crucial role in multiple stages of wound healing. It plays an integral part in blood clot formation, cell proliferation, damaged tissue regeneration and repair, extracellular matrix (ECM) deposition/remodeling/repair, membrane repair as well as its role in modulation of wound-healing process [9]. Zinc’s mechanisms of modulating wound-healing processes is complex: blood coagulation, inflammation, epithelization/granulation tissue formation as well as progress of wound closure [9].

Studies have demonstrated that insufficient zinc intake may contribute to delayed post-neurosurgical wound healing, leading to unnecessary hospital re-admissions for both patient and caretakers. As such, neurosurgeons should recommend topical zinc oxide bandages like Viscopaste or Ichthopaste in order to speed up wound recovery timeframe.

Zinc also modulates immune responses and regulates pro-healing cytokines and growth factors to foster healing. Studies have demonstrated this through zinc supplementation’s promotion of M2 macrophage phenotype, which aids in relieving inflammation by supporting granulation and epithelialization processes; conversely, it suppresses inducible nitric oxide synthase expression associated with M1 macrophages involved in host defense/pathogen clearance functions.

Studies have also shown that zinc increases the number of regulatory T lymphocytes (Tregs), which help to alleviate inflammation and promote wound re-epithelization/granulation [86]. It can also boost activities of many antioxidant enzymes such as superoxide dismutase, catalase, glutathione and malonaldehyde thus inhibiting free radical production which may otherwise hinder healing during the inflammatory phase of wound healing processes [87-90].