Abstract: BACKGROUND: Ginsenoside Rb1 possesses anti-inflammatory and antioxidant effects and can be used to treat tissue cell damage caused by oxidative stress, inflammation, and other related conditions.
OBJECTIVE: To investigate the effect of ginsenoside Rb1 on wound healing in burn rats.
METHODS: Ninety-six Sprague-Dawley rats were randomly divided into control group, model group, low-dose ginsenoside Rb1 group, medium-dose ginsenoside Rb1 group, high-dose ginsenoside Rb1 group, and high-dose ginsenoside Rb1+activator group, with 16 rats in each group. The control group was not modeled, while the other five groups underwent establishment of a dorsal burn model (a 5 cm diameter metal weight heated in 95 °C water was applied vertically to the rat skin for 10 seconds). After modeling, the control and model groups received intraperitoneal injection of normal saline. The low-, medium-, and high-dose ginsenoside Rb1 groups received intraperitoneal injection of 10, 20, and 40 mg/kg ginsenoside Rb1, respectively. The high-dose ginsenoside Rb1+activator group received intraperitoneal injection of 40 mg/kg ginsenoside Rb1 and the Ras homolog gene family member A/Rho-associated coiled-coil kinase (RhoA/ROCK) signaling pathway activator lysophosphatidic acid. All injections were administered once daily for 2 consecutive weeks, and wound healing was observed. After the final administration, samples were collected. Hematoxylin-eosin staining was used to observe wound tissue morphology. TUNEL staining was used to detect the apoptosis rate of wound tissue cells. ELISA was used to measure serum levels of interleukin 6, tumor necrosis factor α, and interleukin 1β. Western blot was used to detect the protein expression of RhoA and ROCK in the wound tissue.
RESULTS AND CONCLUSION: Compared with the control group, the model group showed extensive inflammatory cell infiltration in the wound, incomplete tissue structure, poor epithelial cell growth, and significantly increased apoptosis rate, levels of interleukin 6, tumor necrosis factor α, and interleukin 1β, as well as protein expression of RhoA and ROCK (P < 0.05). Compared with the model group, the low-, medium-, and high-dose ginsenoside Rb1 groups showed no obvious inflammatory cell infiltration in the wound, relatively intact tissue structure, good epithelial cell growth, significantly increased wound healing rate (P < 0.05), and significantly decreased apoptosis rate, levels of interleukin 6, tumor necrosis factor α, and interleukin 1β, as well as protein expression of RhoA and ROCK (P < 0.05), with the most significant changes observed in the high-dose ginsenoside Rb1 group. Compared with the high-dose ginsenoside Rb1 group, the high-dose ginsenoside Rb1+activator group showed obvious inflammatory cell infiltration in the wound, poor tissue structural integrity, poor epithelial cell growth, significantly decreased wound healing rate (P < 0.05), and significantly increased apoptosis rate, levels of interleukin 6, tumor necrosis factor α, and interleukin 1β, as well as protein expression of RhoA and ROCK (P < 0.05). In conclusion, ginsenoside Rb1 may promote wound healing in burned rats by inhibiting the RhoA/ROCK signaling pathway, thereby suppressing inflammatory response and apoptosis.

Key words: burns, ginsenoside Rb1, RhoA/ROCK signaling pathway, wound healing, apoptosis, inflammatory factors