Background: Diabetic nephropathy serves as one of the most regular microvascular complications of diabetes mellitus and is the main factor that causes end-stage renal disease and incident mortality. As the beneficial effect and minute adverse influence of Celastrol on the renal system requires further elucidation, the renoprotective function of Celastrol in early diabetic nephropathy was investigated. Methods: In high-fat and high-glucose diet/streptozotocin-induced diabetic rats which is the early diabetic nephropathy model, ALT, AST, 24 h urinary protein, blood urea nitrogen, and serum creatinine content were observed. Periodic acid-Schiff staining, enzyme-linked immunosorbent assay, immunohistochemical analysis, reverse transcription-polymerase chain reaction, and western blot analysis were used to explore the renoprotective effect of Celastrol to diabetic nephropathy rats and the underlying mechanism. Results: High dose of Celastrol (1.5 mg/kg/d) not only improved the kidney function of diabetic nephropathy (DN) rats, and decreased the blood glucose and 24 h urinary albumin, but also increased the expression of LC3II and nephrin, and downregulated the expression of PI3K, p-AKT, and the mRNA level of NF-κB and mTOR. Conclusion: Celastrol functions as a potential therapeutic substance, acting via the PI3K/AKT pathway to attenuate renal injury, inhibit glomerular basement membrane thickening, and achieve podocyte homeostasis in diabetic nephropathy.

Dendritic cells (DCs) are professional antigen‐presenting cells (APCs) that play a central role in regulating immune responses by linking innate and adaptive immunity. In recent decades, substantial progress has been made in understanding the development, classification, and diverse functions of DCs. However, a comprehensive overview integrating recent advances in the biology and therapeutic targeting of DCs remains lacking. This review systematically summarizes the origin, developmental pathways, and subset heterogeneity of DCs, including classical type 1 and 2 DCs, plasmacytoid DCs, monocyte‐derived DCs, and Langerhans cells. Moreover, it further details the core biological functions of DCs, including antigen capture, migration, and maturation; antigen presentation; activation of adaptive immunity; induction of immune tolerance; and modulation of innate immune responses. The pathological roles of DCs in diseases such as cancer, diabetes, and infectious diseases are discussed, highlighting emerging DC‐based therapeutic strategies. Importantly, this review provides a summary of both preclinical studies and clinical trials involving DC‐targeted therapies, offering a translational perspective. This work aims to deepen the understanding of DC immunobiology and to provide a valuable foundation for the development of novel DC‐based immunotherapies.

In the past few decades, the incidence of liver cancer has been rapidly rising across the world. Rosemary is known to possess antioxidant activity and is used as natural antioxidant food preservative. It is proposed to have anticancer activity in treating different tumor models. In this study, we try to explore the impact of rosemary extracts on upregulating the level of Nrf2 and Nrf2‐regulatory proteins, Sestrin2 and MRP2 in HepG2 cells, and to speculate its potential mechanism. The anticancer activity of rosemary extract, including its polyphenolic diterpenes carnosic acid and carnosol, was evaluated to understand the potential effect on HepG2 cells. Rosemary extract, carnosic acid, and carnosol induced the expression of Sestrin2 and MRP2 associate with enhancement of Nrf2 protein level in HepG2 cells, in which carnosic acid showed most obvious effect. Although the activation pathway of Nrf2/ARE was not exactly assessed, it can be assumed that the enhancement of expression of Sestrin2 and MRP2 may result from upregulation of Nrf2.

Benign prostatic hyperplasia (BPH) is a common disease in the current ageing male population. This research aims to study the effects of Kelong‐Capsules (KLC) on testosterone‐induced BPH. Thirty rats were randomly divided into normal group, model group, and three treatment groups. Three treatment groups were given KLC (3.6 g/kg), KLC (7.2 g/kg), and finasteride (0.9 mg/kg), respectively, for 28 days after establishing the animal model. The BPH rat models were evaluated by Traditional Chinese Medicine (TCM) symptoms and prostate index (PI). Results indicated that three treatment groups all alleviated the pathological changes of prostate and kidney at different levels. Compared with the model group, the PI of the groups treated with KLC (7.2 g/kg) and finasteride decreased significantly. The expressions of NF‐E2 related factor 2 (Nrf‐2) and quinine oxidoreductase (NQO1) in the group treated with KLC (3.6 g/kg) increased markedly (p < 0.01). The cyclooxygenase‐2 (COX‐2) protein expression of the group treated with KLC (7.2 g/kg) was increased (p < 0.01). In conclusion, KLC could obviously inhibit the growth of prostate, and KLC (3.6 g/kg) could promote the expressions of Nrf2 and NQO1.