The Effect and Mechanism of Negative Pressure Wound Therapy on Lymphatic Leakage in Rabbits.

BACKGROUND: Lymphatic leakage is one of the severe complications after lymphadenectomy. However, efficient treatment it still unclear. MATERIALS AND METHODS: We employed inguinal lymphadenectomy and saphenous lymphatic vessel excision to establish a inguinal lymphatic leakage rabbit model. Rabbits with bilateral lymphatic leakage were divided in two groups, which were subject to negative pressure wound therapy (NPWT) on right sides and dressing change on left sides, respectively. Following 7-11 d of treatment, skin thickness and drainage volume were measured. Western blot and RT-PCR were used for analyzing the VEGF-C level. Tissues of wound were dissected and subject to anti-LYVE-1 immunohistochemical for lymphatic average positive staining area percentage and the ratio of lymphatic lumen area evaluation. RESULTS: Our lymphatic leakage model showed significant lymph stasis, delayed wound healing, and skin swelling and was confirmed by methylene blue instillation. Using this rabbit model, we found that NPWT could largely promote wound healing and resolution of skin edema. Compared with the dressing change group, the thickness of the dermis layer in the NPWT group was significantly reduced. Western blot and RT-PCR analysis showed a decrease of VEGF-C in the NPWT group. The immunohistochemical result of the NPWT group did not show a significant change in lymphatic average positive staining area percentage, whereas the ratio of lymphatic lumen area was significantly decreased, suggesting that NPWT treatment can significantly compress the dilated lymphatic vessels. CONCLUSIONS: We successfully established the first clinically relevant lymphatic leakage model in rabbits. NPWT can be an effective treatment for lymphatic leakage via reducing edema and lymphatic stasis by compressing dilated lymph vessels and promoting lymphatic drainage.

Ligustilide treatment promotes functional recovery in a rat model of spinal cord injury via preventing ROS production.

Ligustilide from traditional Chinese medicine extract, angelica sinensis is one of the main active components, and has many pharmacological activities related to the effectiveness. This study sought to determine whether neuro-protection of ligustilide promotes functional recovery in a rat model of spinal cord injury (SCI) via preventing ROS production. Male Sprague-Dawley (SD) rats were induced using operation for model SCI. Furthermore, Basso, Beattie, Bresnahan (BBB) scale and footprint analysis of gait was used to assess the neuro-protection of ligustilide on SCI. The intracellular reactive oxygen species (iROS), prostaglandin E(2) (PGE(2)), interleukin-1ß (IL-1ß) and tumor necrosis factor (TNF)-α production levels were measured by monoclonal enzyme immunoassay kit. Inducible nitric oxide synthase (iNOS) gene expression, activator protein-1 (AP-1) and c-Jun N-terminal kinase (JNK) protein expressions were detected using Quantitative real-time reverse transcription polymerase chain reaction (Q-PCR) and western blot analyses, respectively. Interestingly, treatment with ligustilide significantly increased BBB scale and reduced recovery of coordination in SCI rats. After SCI, the iROS, PGE(2), IL-1ß, TNF-α production levels and iNOS gene expression were significantly suppressed in SCI rats. These results suggest that the neuro-protection of ligustilide promotes functional recovery in a rat model of spinal cord injury via preventing ROS production.