Triclosan (TCS) is a broad-spectrum antimicrobial disinfectant widely used in pharmaceuticals and personal care products (PPCPs). Due to the extensive usage of PPCPs, TCS inevitably entered the environment and posed harmful effects on the ecosystem. Phytoremediation is an attractive approach to remove TCS from the environment. Genetic engineering of plants can be employed to strengthen phytoremediation capacity. In this study, a gene of a nanobody specific to TCS was transformed into Arabidopsis thaliana ( A. thaliana) to enhance the plant absorption of TCS. Two transgenic lines, the T-S-C line with nanobody expression throughout the plant and the T-S-P line with nanobody expression dominant in the roots, were constructed. The expression of nanobody in A. thaliana alleviated the phytotoxicity of TCS. T-S-C and T-S-P exhibited obviously stronger tolerance to TCS toxicity than the wild type (WT), in either a solid medium system or a hydroponics system. Under the stress of TCS, the seedlings of both transgenic plants exhibited an increase of root length and fresh weight compared to those of WT. Moreover, in the presence of TCS, the activities of superoxide dismutase, peroxidase, catalase, and glutathione in transgenic plants were higher than those in WT. The concentration of TCS absorbed by T-S-C and T-S-P from the solid medium system increased by 50.0% and 24.1%, and from the hydroponics system increased by 55.6% and 38.0%, respectively, compared to those absorbed by WT. This study provides a proof of principle that transforming nanobodies into plants represents a novel technology to improve the efficiency of phytoremediation for environmental pollutants.

Background and Purpose: Diabetic nephropathy is one of the most common complications that is related to high morbidity and mortality in type 2 diabetic patients. We investigated ability of a novel dual modulator, PTUPB that concurrently acts as a soluble epoxide hydrolase inhibitor and as a cyclooxygenase-2 inhibitor against diabetic nephropathy. Experimental Approach: Sixteen-week-old type 2 diabetic and proteinuric obese ZSF1 rats were orally treated with vehicle, PTUPB, or enalapril for 8 weeks. Key Results: PTUPB alleviated diabetic nephropathy in obese ZSF1 rats by reducing albuminuria by 50%, renal tubular cast formation by 60-70%, renal fibrosis by 40-50%, glomerular injury by 55% and preserved glomerular nephrin expression. Enalapril demonstrated comparable effects and alleviated diabetic nephropathy in obese ZSF1 rats by reducing all kidney injury parameters by 30 to 50%. Diabetic renal injury in obese ZSF1 rats was accompanied by renal inflammation with 6-7-fold higher urinary MCP-1 level and renal infiltration of CD-68 positive cells. PTUPB and enalapril reduced renal inflammation but PTUPB demonstrated superior anti-inflammatory actions than enalapril. Obese ZSF1 rats were also hypertensive, hyperlipidemic, and exhibited liver injury. Interestingly, PTUPB but not enalapril decreased hyperlipidemia and liver injury in Obese ZSF1 rats. Conclusion and Implication: Overall, we demonstrate that a dual modulator PTUPB does not treat hyperglycemia, but can effectively alleviate hypertension, diabetic nephropathy, hyperlipidemia, and liver injury in type 2 diabetic rats. Therefore, we suggest that PTUPB has promising potential to be developed as a novel therapy for type 2 diabetic nephropathy and other complications.