Background: Inflammatory response plays a crucial role in the occurrence and development of diabetic nephropathy (DN). Drugs that carry anti-inflammatory effects have the potential to treat diabetic nephropathy. It’s reported that alantolactone (ALA), a natural product, has a variety of pharmacological effects against inflammation and oxidation. However, the specific effects of alantolactone on DN and the mechanisms underlying alantolactone remain elusive. Therefore, the present study aimed to probe whether ALA could mitigate inflammation as mediated by high glucose (HG) in NRK-52E cells and reduce renal injury caused by diabetic nephropathy. Materials and methods: The anti-inflammatory effect of ALA was evaluated in the present study using ELISA and RT-qPCR. Western blot and macrophage adhesion assay were then performed to confirm anti-macrophage adhesion and the protein expression of cell adhesion molecules. Finally, the effect of ALA and its underlying mechanism was evaluated in vivo. Results: Results showed that ALA curbed HG-stimulated expression of macrophage adhesion and pro-inflammatory cytokines in renal NRK-52E cells. In addition, both pro-inflammatory cytokines and NF-kappa B witnessed reduced expression or activity in oral administration with ALA in vivo, thus inhibiting the increase of serum creatinine and urea nitrogen (BUN) levels. This in consequence ameliorated fibrosis and stemmed pathological worsening of diabetic renal tissues. Conclusions: These findings suggest that ALA may hold promise in the treatment of DN, and importantly, the anti-inflammatory system may prove to be a new strategy to treat human DN.

In the clinical setting, cisplatin-induced nephrotoxicity primarily manifests as acute kidney injury (AKI). Recent studies have indicated that ferroptosis, a type of iron-dependent cell death, is closely involved in the cisplatin nephrotoxicity. AlkB homologue 5 (ALKBH5), an N6-methyladenosine (m6A) eraser protein expressed in various tissues, including the kidneys, has been implicated in this process. However, the specific role of ALKBH5 in cisplatin-induced nephrotoxicity remains unknown. Our findings indicated that ALKBH5 was upregulated in cisplatin-induced AKI, and the in vivo study results were consistent with the results of the in vitro study. Additionally, ALKBH5 knockout in transgenic animals was found to mitigate cisplatin-induced renal dysfunction, whereas its knock-in exacerbated the effects. Our study revealed that ALKBH5 controls the traditional ferroptosis metabolic pathway, leading to worsening of AKI in experiments conducted both in vivo and in vitro. The efficacy of pharmacological intervention targeting ALKBH5 in AKI animal models was demonstrated, and ALKBH5-based gene therapy confirmed these findings and displayed renoprotective effects against AKI. In conclusion, this study highlighted the crucial role of ALKBH5 as a key regulator of AKI. Overall, our research demonstrates the significant impact of ALKBH5 in controlling ferroptosis in cisplatin-induced AKI, suggesting that focusing on ALKBH5 could be a promising approach for treating cisplatin-related kidney damage. Graphical Abstract

Childhood rhinitis is an inflammatory condition affecting the nasal mucosa of children worldwide. The physical, social, and cognitive performance of children is affected by the chronic symptoms of childhood rhinitis. Effective treatment is essential to avoid long-term effects on children’s lifestyles and well-being. Traditional Chinese medicine (TCM) has been used to treat and prevent several illnesses, and it plays a crucial role in healthcare and rehabilitation. TCM has traditionally been used to holistically treat rhinitis. However, the drawbacks of TCMs, such as their poor water solubility, low bioavailability, single-use, and poor targeting ability, severely restrict their use. In recent years, nanotechnology has been used for various drugs to improve their therapeutic effectiveness and reduce their associated adverse effects. Nanomaterials for TCM formulations are synthesized to be compatible with herbal extracts and sustain active component therapeutic qualities. Nanocarrier-based drug delivery improves bioavailability, circulation time, and targeted distribution, resolving TCM administration issues. This review assesses the innovative combination of TCM and nanotechnology developments for the treatment of childhood rhinitis, providing insights into novel therapeutic approaches. This review also provides significant insights into the potential of this multidisciplinary approach to transform treatment techniques in childhood rhinitis and offers a road map for future research initiatives in this promising sector.

This review examines the distinct mechanisms of Tuina massage and topical herbal medicine in pediatric diarrhea management, focusing on their independent regulation of gastrointestinal metabolism and barrier function. Tuina therapy primarily enhances gastrointestinal motility through the stimulation of targeted acupoints such as Tianshu (ST25) and Shenque (CV8), activating vagal efferent pathways to normalize motility hormones including motilin while suppressing pro-inflammatory cytokines such interleukin-6 and tumor necrosis factor-alpha. It further reinforces mucosal defense by inhibiting mast cell degranulation and augmenting microcirculation via nitric oxide-mediated vasodilation. Herbal medicine containing bioactive compounds from Atractylodes macrocephala and Poria cocos directly restores intestinal barrier integrity by upregulating tight junction proteins occludin and zonula occludens-1, inhibiting epithelial apoptosis, and stimulating MUC2 production. These formulations additionally reprogram enterocyte metabolism by reactivating mitochondrial tricarboxylic acid cycle flux and modulating short-chain fatty acid profiles, with the independent prebiotic effects enhancing commensal butyrate production. Tuina primarily modulates neuroimmune pathways and motility, and herbal medicine directly targets epithelial repair and metabolism. These therapeutic pathways may address core diarrhea pathophysiology, providing holistic complementary therapies. Standardized protocols and interdisciplinary research are urgently needed for clinical translation.

Background and Objectives: This study aimed to explore the risk factors of histopathological crescent formation in pediatric IgA vasculitis nephritis (IgAVN). Materials and Methods: Enrolled patients with biopsy-proven IgAVN from Zhejiang University’s hospital were split into two groups: 377 with no crescents on histopathology (Group 1) and 364 with crescentic nephritis (Group 2). Collected data included clinical features, lab indicators, histopathological grading, and factors causing glomerular sclerosis. Logistic regression was used to assess factors affecting crescent formation in IgAVN. Double-immunofluorescence assay was used to detect TGF-β1, MCP-1, α-SMA, Collagen I, and FN1 in kidney biopsy specimens. The relationship between kidney fibrosis factors and histopathological grade were analyzed using Chi-square and Pearson tests. Results: A total of 741 patients with IgAVN were included in the study. Univariate logistic regression identified potential factors related to crescent formation, including age, gender, clinical classification, hematuria grade, 24 h urine protein level, peripheral white blood cells (WBCs), serum albumin, Cystatin-C, APTT, and PT. Multivariate analysis revealed statistical significance for age, 24 h urine protein, and WBCs across pathological grades (p < 0.05). Mantel–Haenszel Chi-square tests indicated a linear relationship between IgAVN pathological grade and α-SMA, TGF-β1, MCP-1, and FN1. Pearson correlation analysis confirmed a positive correlation between pathological grade and these markers. Conclusions: Age, 24 h urinary protein, and blood WBCs are identified as risk factors for histopathological crescent formation in children with IgAVN. Additionally, a higher pathological grade is associated with more pronounced fibrosis indicators.