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Although antiretroviral therapy has helped to improve the lives of individuals infected with human immunodeficiency virus 1 (HIV-1), these patients are often still afflicted with HIV-1-associated neurocognitive disorders, which can lead to neurocognitive impairment and even dementia, and continue to hamper their quality of life. Methamphetamine abuse in HIV-1 patients poses a potential risk for HIV-associated neurocognitive disorders, because methamphetamine and HIV-1 proteins such as transactivator of transcription can synergistically damage the blood-brain barrier (BBB). In this study, we aimed to examine the effects of methamphetamine and HIV-1 Tat protein on the blood-brain barrier function and to determine whether ginsenoside Rb1 (GsRb1) plays a role in protecting the BBB. Sprague-Dawley rats were divided into four groups. The experimental groups received methamphetamine and HIV-1 Tat protein or both and the control group received saline or GsRb1 pretreatment. Oxidative stress-related factors, tight junction (TJ) proteins, blood-brain barrier permeability, and morphological changes were recorded in each group. The results showed that the group treated with Methamphetamine[Formula: see text]Tat showed a significant change at the ultrastructural level and in the levels of oxidative stress-related factors, TJ proteins, and BBB permeability, suggesting that the BBB function was severely damaged by HIV-1 Tat and methamphetamine synergistically. However, malondialdehyde levels and BBB permeability were lower and the oxidative stress-related factors superoxide dismutase and glutathione were higher in the GsRb1-treated group than in the Methamphetamine[Formula: see text]Tat-treated group, indicating that GsRb1 can protect the BBB against the toxic effects of HIV-1 Tat and methamphetamine. These results show that GsRb1 may offer a potential therapeutic option for patients with HIV-associated neurocognitive disorders or other neurodegenerative diseases.

Periodontitis is the sixth most common chronic inflammatory disease caused by plaque biofilms and closely related to many systemic diseases. In particular, the problems of deep lesion location and sequential treatment of antibacterial and pro-regenerative abilities need to be addressed. We created a novel ROS responsive system (CHX@PCL-PLG) for efficient therapy of refractory periodontitis based on a “three-birds-with-one-stone” strategy, which integrates the biofilm penetration, nitric oxide (NO) sterilization, and NO-mediated pro-angiogenic property into one system. The above system was fabricated by self-assembling vesicles formed by amphiphilic polymers containing poly-ε-caprolactone and guanidinated-poly-ε-lysine as carriers (PCL-PLG) loaded with chlorhexidine (CHX). CHX@PCL-PLG can efficiently penetrate into biofilm under the action of abundant guanidine groups on the vesicle’s surface. Subsequently, the guanidine groups of vesicles respond to the high level of ROS within the biofilm by releasing NO and CHX in a targeted manner to play a synergistic antibacterial and biofilm scavenging function. More importantly, following effective elimination all bacteria from the periodontal pockets, the residual guanidine groups could further produce trace amounts of NO, which promoted angiogenesis and epithelialization of the wound tissue to significantly facilitating wound healing. In conclusion, this study demonstrates that CHX@PCL-PLG makes full use of the characteristics of guanidine groups to significantly disrupt biofilms and promote tissue regeneration for the effective treatment of periodontitis as well as various biofilm-related diseases.