High-Fat Diet and Alcohol Intake Promotes Inflammation and Impairs Skin Wound Healing in Wistar Rats

Abstract

The wound-healing process is complex and remains a challenging process under the influence of several factors, including eating habits. As improper diets may lead to disorders such as dyslipidemia, insulin resistance, and chronic inflammation, potentially affecting the tissue ability to heal, we decided to investigate the effect of a high-fat diet and alcohol intake on the inflammatory process and skin wound healing in Wistar rats. Male rats (n = 30) were individually housed in cages with food and water ad libitum (registration number 213/2014). After anesthesia, at day 40, three circular wounds (12 mm diameter) were made on the back of each animal, which were then randomly assorted into five treatment groups: C1 (control 1)—water via gavage and standard chow diet; C2 (control 2)—water (no gavage) and standard chow diet; AL (alcohol)—water (no gavage) and alcohol (40%) via gavage and standard chow diet; HF (high fat)—water (no gavage) and high-fat diet (50%); and HF + AL (alcohol/high fat)—water (no gavage), alcohol (40%) via gavage, and high-fat diet. Animals were treated for 61 days. Every seven days, the area and the rate of wound contraction were evaluated. Tissue samples were removed for histopathological analysis and biochemical analyses. Our results showed that wound contraction was not complete in the HF + AL rats. Two specific indices of wound-healing impairment (total cell number and levels of the inflammatory cytokine TGF-β) were increased in the HF + AL rats. We also observed decreased type I and III collagen fibers in the HF, AL, and HF + AL groups and increased oxidative stress markers in the same groups. We suggest that a high-fat diet combined with alcohol intake contributed to delayed skin wound healing through increase of the inflammatory phase and promoting oxidative stress, which may have led to morphological alterations and impaired matrix remodeling.

Doxycycline Hyclate Modulates Antioxidant Defenses, Matrix Metalloproteinases, and COX‐2 Activity Accelerating Skin Wound Healing by Secondary Intention in Rats

“…These authors showed that Dx reduced lipid peroxidation in the brain, thus protecting the tissue from the action of free radicals. Another important marker of the action of ROS and RNS in the tissue is the high content of carbonylated protein, which indicates protein oxidation [66,81]. In the present study, after treatment with Dx, only using the lower dose, reduced levels of protein carbonylation were observed, suggesting the antioxidant secondary action of this drug.…”

“…Besides, the formation of new vessels is directly linked to the formation of a new matrix, called granulation tissue, rich in vessels and cells. When the process advances, the number of vessels and cells decreases, but the number of fibers increases, which characterizes mature scar tissue [66]. Therefore, new effective treatments should promote intense neoangiogenesis at the start of the repair pro-cess and reduce the levels of vessels at the end of the process.…”

Nucleoredoxin interaction with flightless‐I/actin complex is differentially altered in alcoholic liver disease

“…It has been shown that acute ethanol exposure reduces collagen content and angiogenesis and as a result delays wound closure in mice 36 . More recently, it has been demonstrated that chronic administration of ethanol in combination with high‐fat diet delays skin wound healing by decreasing collagen type I and III contents, increasing the levels of inflammatory cytokines and promoting oxidative stress 37 . Similarly, ethanol alters several liver homeostatic processes including cytoskeleton contractility and collagen type‐1 content, which drive tissue fibrosis and scar formation 2 .…”

Chronic heavy drinking drives distinct transcriptional and epigenetic changes in splenic macrophages

“…Furthermore, CHD has been associated with poor gastric, dermal, and bone wound healing outcomes [12], increasing the risks for morbidity and mortality following surgery or trauma [13]. Several lines of evidence suggest that this defect is primarily mediated by excessive inflammation associated with CHD, impairing the function of innate immune cells and thus compromising the process of tissue repair [14].…”