BCG-PPD(Beijing Sanroad Biological Products)

The antioxidant 6-PPD has been widely used to prevent cracking and thermal oxidative degradation and to extend the service life of tire rubber. 6-PPD quinone (6-PPDQ) is formed via the reaction of 6-PPD with O₃. Due to its acute lethality in coho salmon, 6-PPDQ has become an emerging pollutant of increasing concern. In this review, we provide a critical overview of the generation, environmental distribution, bioavailability, and potential toxicity of 6-PPDQ. The transformation pathways from 6-PPD to 6-PPDQ include the N-1,3-dimethylbutyl-N-phenyl quinone diamine (QDI), intermediate phenol, and semiquinone radical pathways. 6-PPDQ has been frequently detected in water, dust, air particles, soil, and sediments, indicating its large-scale and potentially global pollution trend. 6-PPDQ is bioavailable to both aquatic animals and mammals and acute exposure to 6-PPDQ can be lethal to some organisms. Exposure to 6-PPDQ at environmentally relevant concentrations could induce several types of toxicity, including neurotoxicity, intestinal toxicity, and reproductive toxicity. This review also identifies and discusses knowledge gaps and research needs for the study of 6-PPDQ. This review facilitates a better understanding of the environmental occurrence and exposure risk of 6-PPDQ.

20(S)-protopanaxadiol (PPD), one of the ginsenosides from Panax ginseng, has been reported to improve performance with dementia. This study aimed to investigate the neuroprotective effect of PPD attenuating NLRP3 inflammasome-mediated microglial pyroptosis in vascular dementia (VD) rats induced by bilateral common carotid artery ligation (2-VO). Male Sprague-Dawley rats (SPF, 150-180 g, n = 10/group) were randomly divided into PPD (20, 10, 5 mg/kg, subcutaneous injection once per day for 3 weeks), model, and vehicle-sham group. It was found that PPD significantly reversed 2-VO-induced cognitive impairment by decreasing escape latency and spontaneous alternation and increasing the number of crossing platforms, showing memory-improving effects. PPD improved the pathological morphology of brain tissue in VD rats. PPD significantly reduced the cerebral infarction area and the activation of microglia in the cortex and hippocampal DG, CA1, and CA3 area. Moreover, PPD could attenuate NLRP3 inflammasome-mediated microglial pyroptosis, inhibit the positive expression of NLRP3, decrease IL-1β, and IL-18 levels, and increase IL-10 levels in the brain cortex. PPD also significantly alleviated the neurotoxicity by decreasing the Aβ and p-Tau in hippocampal DG, CA1, and CA3 areas. In addition, the levels of NLRP3, ASC, and IL-1β in the cortex, APP, BACE1, and p-Tau in the hippocampus were significantly reduced by PPD. These results suggested that PPD hinders microglial activation to alleviate neuroinflammation of NLRP3 inflammasome and inhibits neurotoxicity of Aβ deposition and Tau phosphorylation in 2-VO-induced VD rats.