Illness perception and family resilience in gynaecologic cancer patients: A study on the mediating role of hope.

OBJECTIVE: To investigate the level of family resilience among patients with gynaecologic cancer and explore hope as a mediator between perceptions of illness and family resilience. DESIGN: A cross-sectional study. METHOD: From May to October 2022, researchers used convenience sampling to survey 320 patients with gynaecological cancer at a level 3A hospital in Jinan City. The study instruments included the General Information Questionnaire, Family Hardiness Index, Brief Illness Perception Questionnaire, and Herth Hope Index. SPSS 26.0 was used to analyse the mediation effect of hope. RESULTS: The mean score for family resilience was 55.86 ± 8.62. Illness perception was negatively associated with family resilience, while hope was positively associated with it. Additionally, hope mediated the relationship between illness perception and family resilience. CONCLUSION: There is considerable room for improvement in family resilience among patients with gynaecologic cancer. Interventions aimed at increasing hope can enhance family resilience. IMPACT: Healthcare providers can boost family resilience by fostering hope in patients, thereby promoting effective coping and adaptation to cancer. PATIENT OR PUBLIC CONTRIBUTION: Patients primarily completed the questionnaires, providing insights into the factors that hindered and facilitated the development of family resilience. These findings were communicated to caregivers for further understanding and action.

Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis.

The endoplasmic reticulum (ER) is the main site of protein synthesis, transport, and modification. Its abnormal status has now emerged as an established cause of many pathological processes, such as tumors and autoimmune diseases. Recent studies also demonstrated that the defective functions of ER may lead to pigmentary diseases. Vitiligo is a depigmenting ailment skin disorder whose pathogenesis is now found to be associated with ER. However, the detailed mechanism is still unclear. In this review, we try to link the association between ER with its inter- and intra-organellar interactions in vitiligo pathogenesis and focus on the function, mechanism, and clinical potential of ER with vitiligo. Expand ER is found in melanocytes of vitiligo and ER stress (ERS) might be a bridge between oxidative stress and innate and adaptive immunity. Meanwhile, the tight association between ER and mitochondria or melanosomes in organelles levels, as well as genes and cytokines, is the new paradigm in the pathogenesis of vitiligo. This undoubtedly adds a new aspect to the understanding of vitiligo, facilitating the design of targeted therapies for vitiligo.

GBP2 inhibits pathological angiogenesis in the retina via the AKT/mTOR/VEGFA axis.

Pathological retinal angiogenesis is not only the hallmark of retinopathies, but also a major cause of blindness. Guanylate binding protein 2 (GBP2) has been reported to be associated with retinal diseases such as diabetic retinopathy and hypoxic retinopathy. However, GBP2-mediated pathological retinal angiogenesis remains largely unknown. The present study aimed to investigate the role of GBP2 in pathological retinal angiogenesis and its underlying molecular mechanism. In this study, we established oxygen-induced retinopathy (OIR) mice model for in vivo study and hypoxia-induced angiogenesis in ARPE-19 cells for in vitro study. We demonstrated that GBP2 expression was markedly downregulated in the retina of mice with OIR and ARPE-19 cells treated with hypoxia, which was associated with pathological retinal angiogenesis. The regulatory mechanism of GBP2 in ARPE-19 cells was studied by GBP2 silencing and overexpression. The regulatory mechanism of GBP2 in the retina was investigated by overexpressing GBP2 in the retina of OIR mice. Mechanistically, GBP2 downregulated the expression and secretion of vascular endothelial growth factor (VEGFA) in ARPE-19 cells and retina of OIR mice. Interestingly, overexpression of GBP2 significantly inhibited neovascularization in OIR mice, conditioned medium of GBP2 overexpressing ARPE-19 cells inhibited angiogenesis in human umbilical vein endothelial cells (HUVECs). Furthermore, we confirmed that GBP2 downregulated VEGFA expression and angiogenesis by inhibiting the AKT/mTOR signaling pathway. Taken together, we concluded that GBP2 inhibited pathological retinal angiogenesis via the AKT/mTOR/VEGFA axis, thereby suggesting that GBP2 may be a therapeutic target for pathological retinal angiogenesis.

Zeolitic imidazolate framework-90 loaded with methylprednisolone sodium succinate effectively reduces hypertrophic scar in vivo.

Hypertrophic scar (HS) is characterized by an abnormal fibroblast-myofibroblast transformation; non-apoptosis of fibroblasts; and redundant expression of TGF-ß1, VEGF, α-SMA, and collagen I/III. An HS affects patients' physical and psychological quality of life, leading to joint dysfunction and skin cancer. However, there is currently no satisfactory drug to treat this disorder. In this study, we constructed methylprednisolone sodium succinate (MPSS) encapsulated ZIF-90 (MPSS@ZIF-90) for the effective treatment of an HS. The encapsulation of MPSS in ZIF-90 can achieve the controllable drug release of MPSS and prolong its effective treatment time. MPSS@ZIF-90 enhanced the apoptosis of human hypertrophic scar fibroblasts and downregulated the overexpression of TGF-ß1, VEGF, α-SMA, and collagen I/III both in vitro and in vivo. The instant injection of MPSS@ZIF-90 effectively intervened with the formation of the HS after 28 days. On the contrary, MPSS@ZIF-90 greatly reduced the HS with two injections and 14 days of treatment after the HS was formed. This work provides evidence of effective intervention in the formation of an HS and the therapeutic effectiveness of MPSS@ZIF-90 with short treatment periods in vivo. It suggests that MPSS@ZIF-90 can be used as a biomedical option in the treatment of skin wounds and may reveal the potential molecular basis for promising future antifibrotic agents against scarring.

Untargeted metabolomics yields insight into extramammary Paget's disease mechanisms.

Background: Extramammary Paget's disease (EMPD) is a rare cutaneous malignancy, commonly affecting the external genitalia and perianal area of the elderly with unclear pathogenesis. Metabolomics provides a novel perspective for uncovering the metabolic mechanisms of a verity of cancers. Materials and methods: Here, we explored the metabolome of EMPD using an untargeted strategy. In order to further investigate the potential relationship between metabolites and gene expression, we re-analyzed the gene expression microarray data (GSE117285) using differential expression analysis and functional enrichment analyses. Results: Results showed that a total of 896 metabolites were identified and 87 metabolites including 37 upregulated and 50 downregulated significantly in EMPD were sought out. In the following feature selection analyses, four metabolites, namely, cyclopentyl fentanyl-d5, LPI 17:0, guanosine-3',5'-cyclic monophosphate, kynurenine (KYN, high in EMPD) were identified by both random forest and support vector machine analyses. We then identified 1,079 dysfunctional genes: 646 upregulated and 433 downregulated in EMPD. Specifically, the tryptophan-degrading enzyme including indoleamine-2,3-dioxygenase-1 (IDO1) and tryptophan 2,3-dioxygenase (TDO2) were also increased. Generally, cancers exhibit a high expression of IDO1 and TDO2 to catabolize tryptophan, generating abundant KYN. Moreover, we also noticed the abnormal activation of sustaining proliferative signaling in EMPD. Conclusion: In conclusion, this study was the first to reveal the metabolome profile of EMPD. Our results demonstrate that IDO1/TDO2-initialized KYN metabolic pathway may play a vital role in the development and progression of EMPD, which may serve as a potential therapeutic target for treating EMPD.

Deoxynivalenol exposure induces oxidative stress and apoptosis in human keratinocytes via PI3K/Akt and MAPK signaling pathway.

Deoxynivalenol (DON) is a mycotoxin frequently occurring in human and animal food worldwide, which raises increasing public health concerns. In the present study, we used human keratinocytes (HaCaT cells) as an in vitro model to explore the cytotoxic effect of DON. The results showed that the cells exhibited varying degrees of damage, including decreased cell number and viability, cell shrinkage and floating, when treated with 0.125, 0.25, and 0.5 µg/mL DON for 6, 12, and 24 h, respectively. Furthermore, exposure to DON for 24 h significantly increased the lactate dehydrogenase (LDH) release and intracellular reactive oxygen species (ROS), and prominently decreased the superoxide dismutase (SOD) and catalase (CAT) activity. Additionally, DON exposure induced mitochondrial damage and cell apoptosis through reducing mitochondrial membrane potential. Then, we performed RNA-sequencing to investigate the molecular changes in HaCaT cells after DON exposure. The RNA-sequencing results revealed that DON exposure altered the gene expression involved in apoptosis, MAPK signaling pathway, and PI3K/Akt signaling pathway. Moreover, DON exposure significantly decreased the mRNA and protein expression of Bcl-2, and increased the mRNA and protein expression of Bax, Caspase 3 and COX-2, the protein expression of PI3K, and the phosphorylation levels of Akt, ERK, p38, and JNK. Taken together, these findings suggest that DON exposure could induce cell damage, oxidative stress, and apoptosis in HaCaT cells through the activation of PI3K/Akt and MAPK pathways.

Relationship between illness perception and family resilience in gynecologic cancer patients: the mediating role of couple illness communication.

OBJECTIVE: To analyze the current family resilience levels of Chinese patients with gynecologic cancer and explore the mediating role of couple illness communication between illness perception and family resilience to facilitate patient adaptation to cancer. METHODS: A total of 310 patients with gynecologic cancer were selected from the gynecology ward of a tertiary care hospital in Jinan, Shandong Province, China. All participants provided their demographic and clinical information and completed the Brief Illness Perception Questionnaire (BIPQ), Couples' Illness Communication Scale (CICS), and Family Hardiness Index (FHI). The mediating effect of couple illness communication was analyzed using SPSS26.0 and Amos21.0. RESULTS: The family resilience score of patients with gynecologic cancer was moderate (55.78 ± 8.65). Illness perception was negatively correlated with couple illness communication(p < 0.05) and family resilience(p < 0.01), while couple illness communication was positively correlated with family resilience (p < 0.01). Couple illness communication mediated the relationship between illness perception and family resilience [ß = - 0.071; 95% confidence interval: (- 0.127)-(- 0.013)]. CONCLUSIONS: The family resilience of patients with gynecologic cancer must be further improved. Since couple illness communication mediates the relationship between illness perception and family resilience in this population, it is important to improve patients' illness perceptions and couple illness communication to enhance their family resilience.

Couple communication quality and family resilience among Chinese gynecologic cancer patients and their spouses: a dyadic study.

PURPOSE: The purpose of this study was to explore the couple communication process for gynecologic cancer (GC) patients and their spouses. Particular attention was given to examining the relationship between couple communication quality and family resilience for GC dyads. METHODS: In this cross-sectional study, 354 dyads were recruited from a gynecology ward of a public hospital in China. The patients and their spouses completed the Couples' Communication Quality Scale and the Family Hardiness Index. This study used the actor-partner interdependence model (APIM) to examine the effect of couple communication quality on family resilience in distinguishable GC dyads. RESULTS: Both GC patients and their spouses reported a moderate level of couple communication quality and family resilience, but spouses reported better couple communication and family resilience than patients. With the exception of perceived response, for which only a patient actor effect was observed, the factors of couple communication quality had significant actor effects on family resilience for both patients and spouses. Additionally, four significant partner effects were found: spouse self-disclosure, stress coping, and productive action positively predicted patients' family resilience, while patient normalcy crafting positively predicted spouses' family resilience. CONCLUSION: This study not only highlights the need for couple-based communication strategies for developing family resilience but also identifies differences in the experiences of patients and their partners, which provides a direction for future intervention research. Through the development of interventions at a dyadic level, spouses can be encouraged to actively engage in communication, which may promote mutual family resilience in a larger sense.

Triptolide Induces Apoptosis and Autophagy in Cutaneous Squamous Cell Carcinoma via Akt/mTOR Pathway.

BACKGROUND: Tripterygium wilfordii Hook F provided the source of the first diterpenoid triepoxide lactone, Triptolide, identified as the primary constituent causing the anticancer activity. So far, it has not been reported whether triptolide has a therapeutic effect on cutaneous squamous cell carcinoma (cSCC). OBJECTIVE: This study investigates the triptolide's therapeutic impact on cSCC both in vitro and in vivo and investigates the triptolide's potential involvement in signaling pathways. METHODS: The CCK-8 assays, wound healing assays, and colony formation assays were used to assess the effects of triptolide on the proliferation and migration of cSCC cells. The alteration in gene expression following triptolide treatment was shown by RNA sequencing. Flow cytometry was then applied to evaluate cell apoptosis. Western blot was used to find the associated proteins' expressions. The effectiveness of triptolide was then evaluated in vivo using a xenograft model, and histological staining was employed to determine the visceral toxicity. RESULTS: Triptolide greatly reduces the migratory and proliferative capacity of cSCC cells. Triptolide dramatically decreased cell viability and migration in the A431 and SCL-1 cells compared to the control group, according to the CCK8 assay, wound healing assay, and colony formation assay. Flow cytometry demonstrated that treatment with 10- 40 nM triptolide increased apoptosis in a concentration-dependent manner, with a statistically significant difference. Furthermore, mice given triptolide had smaller tumor sizes than those in the control group. Triptolide treatment drastically altered the expression of autophagic and apoptotic proteins. The considerable reduction in the proteins Akt and mTOR levels further illustrated the critical function of triptolide in cSCC. CONCLUSION: Triptolide caused cSCC cells to engage in autophagy and apoptosis by inhibiting the Akt/mTOR signaling pathways. Triptolide may be a possible antitumor agent for the treatment of cSCC.

A three-dimensional printed assembled sleeveless guide system for fiber-post removal.

This report describes a technique to develop a three-dimensional printed assembled sleeveless guide system to aid the fiber-post removal in a safe and efficient way. The surface and volume data of the dentition containing the targeted tooth were acquired with optical scanners and cone-beam computed tomography. The virtual path of the fiber-post removal was determined and integrated with a guide prototype with a cylindrical passage. The prototype data was split into two separate parts, combined with the matched pin and jack structures to facilitate the assembly. A guide tube was generated based on the axis of the cylindrical passage, split into three units, and combined with the previously processed data with connectors to form the finalized guide system. The adaptor for the head of handpiece was designed to facilitate the guidance. All the finalized data were printed with titanium alloy. The fiber-post of the upper right central incisor was successfully removed with the aid of this assembled sleeveless guide system that guides the handpiece rather than the rotary instrument.

Dyadic communication quality and family resilience in gynecologic cancer survivors: a study on the mediating role of perceived spousal support.

PURPOSE: To analyze the level of family resilience in Chinese gynecological cancer survivors and determine whether perceived spousal support plays a mediating role in the relationship between dyadic communication quality and family resilience, enhance the confidence of families in coping with the disease together, and thus promote psychosocial adaptation to cancer. METHODS: A total of 348 gynecologic cancer survivors were selected from a gynecologic ward in a public hospital in Shandong Province, China. All participants completed the Sociodemographic and Clinical Characteristics Questionnaire, Couples' Communication Quality Scale (CCQS), Perceived Social Support Scale (PSSS), and Family Hardiness Index (FHI). The mediating effect of perceived spousal support was estimated using the bootstrap method via IBM SPSS AMOS 21.0. RESULTS: The mean FHI score was 53.03 ± 9.34 points, showing moderate levels of family resilience. Family resilience was shown to be significantly positively associated with both perceived spousal support and dyadic communication quality (both p < 0.01). Furthermore, perceived spousal support was shown to partially mediate the relationship between communication quality and family resilience (ß = 0.141; 95% confidence interval: 0.063-0.243). CONCLUSION: The level of family resilience in survivors of gynecologic cancer needs to be further improved, and perceived spousal support partially mediates the relationship between dyadic communication quality and family resilience within this population. Therefore, dyadic communication quality and subjective perceived spousal support should be enhanced for gynecologic cancer survivors to increase their family resilience.

MCPIP1 promotes cell proliferation, migration and angiogenesis of glioma via VEGFA-mediated ERK pathway.

Glioma is the most common primary malignant intracranial tumor in the population, and is often associated with abundant angiogenesis. However, how angiogenesis is regulated during glioma progression is still poorly understood. Data mining of cancer patient database shows that MCPIP1 is positively correlated with VEGFA expression and negatively with survival. In this study, we report that overexpressed MCPIP1 in glioma cells is a boost of angiogenesis. Mechanistically, MCPIP1 upregulates the expression of VEGFA in glioma, and promote the secretion of VEGFA to the surroundings, which could stimulate angiogenesis through ERK pathway. Blocking VEGFA expression and secretion inhibited MCPIP1-mediated angiogenesis and glioma progression in vitro and xenograft models. Collectively, these results identify a critical role for MCPIP1 in angiogenesis and glioma progression by regulating the VEGFA-mediated ERK pathway, suggesting that targeting MCPIP1 may be a potential glioma-selective therapeutic strategy.

Genistein reverses the effect of 17ß-estradiol on exacerbating experimental occlusal interference-induced chronic masseter hyperalgesia in ovariectomised rats.

BACKGROUND: Oro-facial pain is more prevalent in women than in men, and oestrogen may underlie this sex difference. Genistein reversed the potentiation of 17ß-estradiol (E2) on glutamate-induced acute masseter nociceptive behaviour, but its role in dental experimental occlusal interference (EOI)-induced chronic masseter hyperalgesia remains unclear. OBJECTIVE: This study aimed to investigate sex differences, and to explore the role and underlying mechanisms of genistein in E2-potentiated EOI-induced chronic masseter hyperalgesia in rats. METHODS: Female and male rats were prepared to compare the sex differences of masseter hyperalgesia induced by EOI using a 0.4-mm-thick metal crown. Female rats were ovariectomised (OVX) and treated with E2 and genistein, followed by EOI. The head withdrawal threshold (HWT) was examined to assess masseter sensitivity. The protein expression of transient receptor potential vanilloid-1 (TRPV1) in the trigeminal ganglion (TG) was detected using western blotting. Immunofluorescence staining was used to reveal the colocalisation of oestrogen receptors (ERs) with TRPV1 and the percentage of TRPV1-positive neurons in the TG. RESULTS: To some extent, female rats displayed enhanced sensitivity to EOI-induced chronic masseter hyperalgesia compared with males. Female rats showed the lowest HWT in the pro-oestrus phase. Pre-treatment with genistein antagonised E2 potentiation in EOI-induced masseter hyperalgesia and blocked the effect of E2 by downregulating TRPV1 protein expression and the percentage of TRPV1-positive neurons in the TG. CONCLUSION: Female rats showed greater masseter hyperalgesia than males under EOI. Genistein antagonised the facilitation of EOI-induced chronic masseter hyperalgesia by E2 probably through inhibiting TRPV1 in the TG.

Stem Cell-Based Therapies in Hearing Loss.

In recent years, neural stem cell transplantation has received widespread attention as a new treatment method for supplementing specific cells damaged by disease, such as neurodegenerative diseases. A number of studies have proved that the transplantation of neural stem cells in multiple organs has an important therapeutic effect on activation and regeneration of cells, and restore damaged neurons. This article describes the methods for inducing the differentiation of endogenous and exogenous stem cells, the implantation operation and regulation of exogenous stem cells after implanted into the inner ear, and it elaborates the relevant signal pathways of stem cells in the inner ear, as well as the clinical application of various new materials. At present, stem cell therapy still has limitations, but the role of this technology in the treatment of hearing diseases has been widely recognized. With the development of related research, stem cell therapy will play a greater role in the treatment of diseases related to the inner ear.

17ß-Estradiol Exacerbated Experimental Occlusal Interference-Induced Chronic Masseter Hyperalgesia by Increasing the Neuronal Excitability and TRPV1 Function of Trigeminal Ganglion in Ovariectomized Rats.

Pain symptoms in temporomandibular disorders (TMD) predominantly affect reproductive women, suggesting that estrogen regulates pain perception. However, how estrogen contributes to chronic TMD pain remains largely unclear. In the present study, we performed behavioral tests, electrophysiology, Western blot and immunofluorescence to investigate the role and underlying mechanisms of estrogen in dental experimental occlusal interference (EOI)-induced chronic masseter mechanical hyperalgesia in rats. We found that long-term 17ß-estradiol (E2) replacement exacerbated EOI-induced masseter hyperalgesia in a dose-dependent manner in ovariectomized (OVX) rats. Whole-cell patch-clamp recordings demonstrated that E2 (100 nM) treatment enhanced the excitability of isolated trigeminal ganglion (TG) neurons in OVX and OVX EOI rats, and EOI increased the functional expression of transient receptor potential vanilloid-1 (TRPV1). In addition, E2 replacement upregulated the protein expression of TRPV1 in EOI-treated OVX rats. Importantly, intraganglionic administration of the TRPV1 antagonist AMG-9810 strongly attenuated the facilitatory effect of E2 on EOI-induced masseter mechanical sensitivity. These results demonstrate that E2 exacerbated EOI-induced chronic masseter mechanical hyperalgesia by increasing TG neuronal excitability and TRPV1 function. Our study helps to elucidate the E2 actions in chronic myogenic TMD pain and may provide new therapeutic targets for relieving estrogen-sensitive pain.

Development and validation of a survival model for thyroid carcinoma based on autophagy-associated genes.

Abnormalities in autophagy-related genes (ARGs) are closely related to the occurrence and development of thyroid carcinoma (THCA). However, the effect of ARGs on the prognosis of THCA remains unclear. Here, by analyzing data from TCGA, 26 differentially expressed ARGs were screened. Cox regression and Lasso regression were utilized to analyze the prognosis of the training group, and a risk model was constructed. Our results show that low-risk patients had better overall survival (OS) than high-risk patients, and the area under the ROC curve in the training and testing groups was significant (3-year AUC, 0.735 vs 0.796; 5-year AUC, 0.821 vs 0.804). In addition, a comprehensive analysis of the 5 identified ARGs demonstrated that most of them were related to OS in THCA patients, and two of them (CX3CL1 and CDKN2A) were differentially expressed in THCA and normal thyroid tissues at the protein level. GSEA suggested that the inactivation of the cell defense system and the activation of some classical tumor signaling pathways are important driving forces for the progression of THCA. This study demonstrated that the 5 ARGs in the survival model are promising multidimensional biomarkers for the diagnosis, prognosis, and treatment of THCA.

Effect of chlorogenic acid on alleviating inflammation and apoptosis of IPEC-J2 cells induced by deoxyniyalenol.

Deoxynivalenol (DON) is extensively detected in many kinds of foods and feeds to harm human and animal health. This research aims to investigate the effect of chlorogenic acid (CGA) on alleviating inflammation and apoptosis of swine jejunal epithelial cells (IPEC-J2) triggered by DON. The results demonstrated that cell viability was decreased when DON concentrations increased or incubation time expanded. The pretreatment with CGA (40 µg/mL) for 1 h increased cell viability, decreased lactate dehydrogenase (LDH) release and apoptosis in cells triggered by DON at 0.5 µg/mL for 6 h, compared with the DON alone-treated cells. Moreover, the mRNA abundances of IL-8, IL-6, TNF-α, COX-2, caspase-3, Bax and ASCT2 genes, and protein expressions of COX-2, Bax and ASCT2 were significantly down-regulated; while the mRNA abundances of ZO-1, claudin-1, occludin, PePT1 and GLUT2 genes, and protein expressions of ZO-1, claudin-1 and PePT1 were significantly up-regulated in the CGA + DON group, compared with the DON alone group. This study indicated that CGA pretreatment alleviated cytotoxicity, inflammation and apoptosis in DON-triggered IPEC-J2 cells, and protected intestinal cell integrity from DON damages.

[The status of ENT health care workers at the forefront of fighting against COVID-19 in Wuhan and some response options].

It is a critical period of fighting against new coronavirus（SARS-CoV-2） disease now，since its outbreak on December 2019 in Wuhan.Even though the front line staffs are thought heroes，the ENT doctors and nurses are also indispensable power in defending the disease.The number of outpatients of ENT is huge.The early stage of SARS-CoV-2 pneumonia（COVID-19） may present pharyngalgia or cough without fever.Thus，the ENT doctors have high risks of being consulted by early stage COVID-19 patients.This paper means to talk about the contributions of ENT doctors and nurses in defending against SARS-CoV-2 virus，as well as the mental status of them.

Effects of Compound Active Peptides on Protecting Liver and Intestinal Epithelial Cells from Damages and Preventing Hyperglycemia.

Active peptides have good effectiveness in controlling or preventing many diseases. Compound active peptides (CAP) obtained from animal, plant, and sea food proteins were used in this study to explore their effects on antioxidation, anti-inflammation, and antihyperglycemia in vitro and in vivo. The results demonstrated that 10 µg/mL CAP could increase cell viability (P < 0.05) and decrease reactive oxygen species (ROS) levels and cell apoptosis (P < 0.05) when WRL68 cells were induced by H2O2 for 6 h. Moreover, incubation with 20 µg/mL CAP for 6 h significantly increased cell viability and Bcl-2 expression level (P < 0.05) and decreased expression levels of IL-6, IL-8, TNF-α, Bax, and Caspase 3 and the ratio of Bax/Bcl-2 (P < 0.05) when swine jejunal epithelial cells (IPEC-J2) were induced by deoxynivalenol (DON). In addition, adding CAP individually or combined with Liuweidihuang pills (LDP, Chinese medicine) and low-dose glibenclamide could lower blood glucose levels in alloxan-induced hyperglycemic model mice. These results suggested that CAP was probably a beneficial ingredient for alleviating H2O2-induced oxidative stress and DON-induced cell inflammation and apoptosis and preventing hyperglycemia.

Astilbin ameliorates deoxynivalenol-induced oxidative stress and apoptosis in intestinal porcine epithelial cells (IPEC-J2).

Deoxynivalenol (DON) is a common mycotoxin, which often induces oxidative stress and cytotoxicity in humans and animals. Astilbin (AST), as a natural antioxidant, exhibits multiple pharmacological functions. The aim of this study was to investigate the effects of AST on alleviating DON-induced cytotoxicity in intestinal porcine epithelial cells (IPEC-J2). The results demonstrated that 0.5 µg/mL DON stimulation for 6 hours induced oxidative stress, inflammation and apoptosis in IPEC-J2 cells. AST enhanced the cell viability in a dose- and time-dependent manner. The addition of 20 µg/mL AST significantly increased cell viability, superoxide dismutase and catalase activities, Bcl-2 gene expression and the Bcl-2/Bax ratio (P < .05), and decreased lactate dehydrogenase release, malondialdehyde content and the relative expressions of genes associated with inflammation and apoptosis such as interleukin-6 and -8, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, Bax and caspase-3 (P < .05). Simultaneously, zonula occludens-1, claudin-1 and PepT1 gene expressions were upregulated and occludin, ASCT2 and GLUT2 gene expressions were downregulated by the addition of AST, compared with the DON group (P < .05). These results indicated that 20 µg/mL AST could ameliorate oxidative stress, inflammation and apoptosis by enhancing antioxidant enzyme activities and intestinal barrier function, and reducing the expressions of inflammation and apoptosis genes, as well as improve the barrier function and nutrient transport and absorption in DON-induced IPEC-J2 cells.