Radix Hedysari polysaccharides(Radix Hedysari polysaccharides) - 在研适应症：放射性直肠损伤_专利_临床

概要

基本信息

药物类型

化学药、糖类药物

别名

HPS

靶点-

作用方式-

作用机制-

治疗领域

消化系统疾病

在研适应症

放射性直肠损伤

非在研适应症-

原研机构

甘肃中医药大学

在研机构

甘肃中医药大学

非在研机构-

权益机构-

最高研发阶段临床前

首次获批日期-

最高研发阶段(中国)临床前

特殊审评-

关联

100 项与 Radix Hedysari polysaccharides 相关的临床结果

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100 项与 Radix Hedysari polysaccharides 相关的转化医学

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100 项与 Radix Hedysari polysaccharides 相关的专利（医药）

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50

项与 Radix Hedysari polysaccharides 相关的文献（医药）

2025-09-01·INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

Protective effect of HPS against irinotecan-induced intestinal injury in drosophila and mice via modulation of inflammation, oxidation, and gut microbiota

Article

作者: Du, Xianqin ; Chen, Qiqi ; Zhang, Li ; Lin, Xingyao ; Han, Shuzhen ; Li, Botong ; Li, Shuang ; Xiu, Minghui ; Gao, Rongni ; Li, Liangliang ; He, Jianzheng

Intestinal mucositis is a common and debilitating complication of the chemotherapeutic agent irinotecan (CPT-11), characterized by intestinal barrier disruption, oxidative stress, inflammation, and gut microbiota dysbiosis. Radix Hedysari polysaccharides (HPS) possess anti-inflammatory, antioxidant, and microbiota-regulating properties, but their protective effects against CPT-11-induced intestinal injury remain unclear. In this study, we investigated the protective effect and mechanism of HPS in CPT-11-induced intestinal mucositis using Drosophila melanogaster and BALB/c mouse models. HPS supplementation significantly improved survival and locomotor activity in CPT-11-induced flies, and ameliorated intestinal phenotypes including excessive feeding, increased excretion, crop enlargement, shortened gut length, impaired acid-base balance, and elevated intestinal cell death. HPS also suppressed reactive oxygen species (ROS) levels and modulated antioxidant-related genes (gstD1, cat, sod1, sod2) and the JAK pathway (STAT92E, UPD3, UPD3-1) in fly guts. In mice, administration of HPS reversed the CPT-11-induced gut microbial dysbiosis, restored microbial diversity, and suppressed serum pro-inflammatory cytokines (TNF-α and IL-6). Mechanistic studies revealed that HPS alleviated colonic injury by up-regulating the Keap1/Nrf2 antioxidant response and down-regulating the JAK1/STAT6 inflammatory signaling. These findings suggest that HPS has a protective role in CPT-11-induced intestinal mucositis via antioxidant, anti-inflammatory, and microbiota-modulatory activities, supporting its potential as a therapeutic agent for chemotherapy-induced intestinal injury.

2025-03-01·LIFE SCIENCES

Hyperoside mitigates PCOS-associated adipogenesis and insulin resistance by regulating NCOA2-mediated PPAR-γ ubiquitination and degradation

Article

作者: Ouyang, Xiaoling ; Wang, Yongfeng ; Zhou, Qi ; Li, Linxia ; Tang, Hong ; Hua, Yu

AIMS:

Polycystic ovary syndrome (PCOS) is closely associated with metabolic disorders such as insulin resistance and obesity, but the role of adipogenesis in its pathophysiology remains unclear. This study investigates the role of adipogenesis in PCOS development and evaluates whether hyperoside (HPS), an anti-adipogenic herbal compound, can improve PCOS by inhibiting adipogenesis.

MAIN METHODS:

A combination of in vivo and in vitro models was used to assess the impact of HPS on ovarian function, insulin resistance, and adipogenesis. PCOS mice were treated with HPS, and their ovarian function and insulin resistance were evaluated. In vitro adipocyte differentiation assays were conducted to examine the effects of HPS on adipogenesis. The target of HPS was analyzed by Surface plasmon resonance. The expression levels of NCOA2 and PPAR-γ ubiquitination and degradation were analyzed using quantitative real-time PCR and Western blotting. Additionally, NCOA2 knockdown experiments were performed to investigate its role in ovarian function, insulin resistance, and adipogenesis in PCOS mice.

KEY FINDINGS:

HPS treatment significantly improved ovarian function, reduced insulin resistance, and suppressed adipogenesis in PCOS mice. Mechanistically, HPS inhibited adipogenesis by reducing NCOA2 expression, thereby preventing PPAR-γ ubiquitination and degradation. Knockdown of NCOA2 further validated its role by improving ovarian function, insulin resistance, and adipogenesis in PCOS models.

SIGNIFICANCE:

These findings demonstrate that HPS alleviates PCOS by regulating NCOA2-mediated PPAR-γ ubiquitination and degradation, offering new insights into the role of adipogenesis in PCOS pathophysiology.

2025-01-01·Iranian Journal of Basic Medical Sciences

Potential therapeutic effects of shrimp protein hydrolysates on NAFLD-induced infertility disorders: Insights into redox balance, heat shock protein expression, and chromatin compaction in male rats.

Article

作者: Razi, Mazdak ; Najdegerami, Ebrahim ; Rahmani, Somayyeh ; Nikoo, Mehdi

Objectives:

Nonalcoholic fatty liver disease (NAFLD) is known to disrupt testicular anti-oxidant capacity, leading to oxidative stress (OS) that can negatively affect male fertility by damaging sperm DNA. Heat shock proteins (HSP70 and HSP90), in association with transitional proteins (TP1 and TP2), play crucial roles in protecting sperm DNA integrity in oxidative conditions. Whiteleg shrimp protein hydrolysates (HPs) exhibit anti-oxidant properties, prompting this study to explore the potential of HPs in ameliorating NAFLD-induced testicular damage.

Materials and Methods:

The study divided rats into four groups: control, a group subjected to a high-fat diet (HFD) to induce NAFLD without supplementation, and two HFD-induced NAFLD groups receiving HP doses (20 and 300 mg/kg). After 70 days, the testicular total anti-oxidant capacity (TAC), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), HSP70-2a, HSP90 expression, and TP mRNA levels were assessed.

Results:

The results showed that HFD-induced NAFLD significantly increased GSH and MDA levels and disrupted the GSH/GSSG ratio (P<0.05) while also reducing HSP70-2a, HSP90, TP1, and TP2 expression (P<0.05). However, HP administration effectively restored testicular redox balance, reduced oxidative stress, and enhanced these protective proteins' expression compared to HFD (P<0.05).

Conclusion:

NAFLD negatively affects the testicular redox system and HSP and TP expression, disrupting male fertility potential. In contrast, HP-treated rats showed a marked effect on NAFLD-induced damage by improving testicular anti-oxidant status and regulating the expression of HSPs and TP proteins. These findings suggest a potential therapeutic role for HP in safeguarding male fertility against the damaging effects of NAFLD.

100 项与 Radix Hedysari polysaccharides 相关的药物交易

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