Stress In Spleen Tissues Research Articles

Short-term immunotoxicity induced by florpyrauxifen-benzyl herbicide exposure in the spleen of male albino mice.

Florpyrauxifen-benzyl (FPB)is a new arylpicolinate systemic herbicide that has been used to control or suppress the majority of herbicide-resistant biotype weeds in rice. To our knowledge, the impact of FPB on the immune system remains undetected thus far. Hence, this work aimed to address the toxic effects of FPB and the possible related mechanisms on the spleen of exposed mice. Initially, an acute toxicological test was performed to ascertain the median lethal dose (LD50) of FPB for 24 h which was found to be 371.54 mg/kg b.wt. For mechanistic evaluation of FPB toxicity, three sublethal doses (1/20th, 1/10th, and 1/5thLD50) were orally administered to mice for 21 consecutive days. Changes in spleen relative weight, oxidative status, apoptotic and inflammatory markers, histopathological alterations were evaluated. Following the FPB exposure, significant (p < 0.05) decline in spleen index, apoptotic features, histolopathological changes were observed. Additionally, excessive oxidative stress in spleen tissues was monitored by downregulating antioxidant enzymes and upregulating the oxidant parameters. Furthermore, exposure to FPB resulted in notable activation of the NF-қB signaling pathway, accompanied by elevated levels of pro-inflammatory cytokines (namely, IL-1βand TNF-α)as well as CD3 and CD19 levels have decreased significantly in spleen tissues. Collectively, FPB exposure exhibited apoptosis, oxidative stress, immunosuppression, and inflammatory response in a dose-dependent manner, leading to spleen tissue damage and immunotoxicity. Further studies on FPB is recommended to outstand its hazards on ecosystems.

Liensinine attenuates inflammation and oxidative stress in spleen tissue in an LPS-induced mouse sepsis model.

Sepsis is a complex syndrome caused by multiple pathogens and involves multiple organ failure, particularly spleen dysfunction. In 2017, the worldwide incidence was 48.9 million sepsis cases and 11 million sepsis-related deaths were reported (Rudd et al., 2020). Inflammation, oxidative stress, and apoptosis are the most common pathologies seen in sepsis. Liensinine (LIE) is a bisbenzylisoquinoline-type alkaloid extracted from the seed embryo of Nelumbo nucifera. Lotus seed hearts have high content of LIE which mainly has antihypertensive and antiarrhythmic pharmacological effects. It can exert anti-carcinogenic activity by regulating cell, inflammation, and apoptosis signaling pathways (Manogaran et al., 2019). However, its protective effect from sepsis-induced spleen damage is unknown. In this research, we established a mouse sepsis model induced by lipopolysaccharide (LPS) and investigated the protective effects of LIE on sepsis spleen injury in terms of inflammatory response, oxidative stress, and apoptosis.

Valproic Acid Attenuates Oxidative Damage in Rat Spleen Tissue Induced By Spinal Cord Damage

Events such as oxidative stress caused by spinal cord injury (SCI) are a serious condition because they negatively affect many organs. Alternative treatment options for this type of injury are quite limited. In this study, we planned to investigate the effect of oxidative damage on the spleen tissue of rats with spinal cord damage and the protective role of valproic acid (VPA) in this damage. Sixteen Wistar albino rats were divided into two equal groups. No treatment was administered to the rats in Group 1 (SCI-(Control), but a single dose of 300 mg/kg intraperitoneally VPA was administered to the rats in Group 2 (SCI-VPA). Superoxide dismutase (SOD) activities, total antioxidant status (TAS) and total oxidant status (TOS) levels were examined as markers of oxidative stress in spleen tissues taken after decapitation of rats. VPA treatment increased the SOD and TAS level but decreased the TOS level, indicating improved oxidative damage and impaired enzymatic antioxidant levels in spleen tissue homogenate damaged by SCI. We have observed that VPA, which has many beneficial properties, has a significant healing effect on spleen tissue affected by SCI-induced oxidative stress.

Dietary curcumin supplementation can enhance health and resistance to ammonia stress in the greater amberjack (Seriola dumerili)

We evaluated the effect of dietary curcumin supplementation on the antioxidant capacity of the liver and the resistance of the liver and spleen to ammonia stress in the great amberjack (Seriola dumerili). Three isonitrogenous and isolipidic test diets were prepared by supplementing incremental levels of dietary curcumin at 0 mg/kg (CUR0%, control), 100 mg/kg (CUR0.01%), and 200 mg/kg (CUR0.02%), respectively. Each diet was randomly assigned to triplicate groups of 15 fish per tank. At the end of the feeding experiment, dietary curcumin supplementation positively modulated antioxidant-related genes and enzyme activity in liver tissues. After the ammonia challenge, dietary supplementation with the appropriate level of curcumin alleviated ammonia stress in liver tissue by upregulating the relative expression of GSH-Px and downregulating the relative expression of Keap1 and GR. Meanwhile, ammonia stress in spleen tissue could also be alleviated by upregulating the relative expression of CAT, downregulating the relative expression of GR, and increasing the activity of SOD and GSH. After the recovery, dietary supplementation with curcumin still alleviated ammonia stress in the liver tissue by upregulating the relative expression of CAT, downregulating the relative expression of Keap1 and GR, and increasing the activity of SOD and GSH. On the other hand, ammonia stress in spleen tissue was still alleviated by upregulating the relative expression of Mn-SOD and increasing the activity of SOD and GSH. The histological structure results also showed that liver cells in the curcumin-containing groups exhibited a positive impact on cell boundaries, alignment, and nuclei after the ammonia challenge and recovery. Spleen cells in the curcumin-containing groups exhibited greater aggregation of melano-macrophage centers after the ammonia challenge and recovery. These results suggest that dietary curcumin supplementation at 100 mg/kg can promote the health condition and resistance to ammonia stress of the greater amberjack.

The Protective Effects of Vitamins A and E on Titanium Dioxide Nanoparticles (nTiO2)-Induced Oxidative Stress in the Spleen Tissues of Male Wistar Rats.

Titanium dioxide nanoparticles (nTiO2) can accumulate in different tissues and damage them with oxidative stress induction. Different components with antioxidant capacity can protect the tissues. So in this study, the protective effects of vitamin A and E on the nTiO2-induced oxidative stress in rats' spleen tissues were examined. Thirty-six male Wistar rats were randomly divided into 6 groups: Control 1 (received water), nTiO2, nTiO2 + vitamin E, nTiO2 + vitamin A, nTiO2 + vitamin A and E, and Control 2 (received olive oil). To investigate the status of oxidative stress, total antioxidant capacity (TAC), total oxidant status (TOS), and lipid peroxidation (LPO) were determined in spleen tissue as well as the activities of antioxidant enzymes, including glutathione peroxidase (GPx) and superoxide dismutase (SOD). Also, the gene expression of GPx, SOD, and nuclear factor-E2-related factor-2 (Nrf-2) were determined by qRT-PCR. To evaluate the spleen histopathological changes, H&E staining was carried out. nTiO2 significantly increased TOS and LPO levels, whereas it decreased TAC level, GPx and SOD activities, and gene expression of GPx, SOD, and Nrf-2 in spleen tissues of rats compared with controls (p < 0.05). In vitamin-treated rats, the levels of TOS and LPO significantly decreased, and the level of TAC, the activities of GPx and SOD, and the gene expression of GPx, SOD, and Nrf-2 increased compared to nTiO2 group (p < 0.05). These parameters are maintained near to normal levels. Histological findings confirmed the protective effects of these vitamins on tissue damage caused by nTiO2. Vitamin A and E can protect the spleen tissues from nTiO2-induced oxidative stress.

The role of heat shock protein 70 in oxidant stress and inflammatory injury in quail spleen induced by cold stress.

The aim of this study was to investigate the role of heat shock protein 70 (Hsp70) in oxidative stress and inflammatory damage in the spleen of quails which were induced by cold stress. One hundred ninety-two 15-day-old male quails were randomly divided into 12 groups and kept at 12 ± 1°C to examine acute and chronic cold stress. We first detected the changes in activities of antioxidant enzymes in the spleen tissue under acute and chronic cold stress. The activities of glutathione peroxidase (GSH-Px) fluctuated in acute cold stress groups, while they were significantly decreased (p < 0.05) after chronic cold stress. The activities of superoxide dismutase (SOD), inducible nitric oxide synthase (iNOS), and nitric oxide (NO) content were decreased significantly (p < 0.05) in both of the acute and chronic cold stress groups. Malondialdehyde (MDA) content was significantly increased (p < 0.05) under cold stress except the 0.5h group of acute cold stress. Besides, histopathological analysis showed that quail's spleen tissue was inflammatory injured seriously in both the acute and chronic cold stress groups. Additionally, the inflammatory factors (cyclooxygenase-2 (COX-2), prostaglandin E synthase (PTGES), iNOS, nuclear factor-kappa B (NF-κB), and tumor necrosis factor-a (TNF-α)) and Hsp70 mRNA levels were increased in both of the acute and chronic cold stress groups compared with the control groups. These results suggest that oxidative stress and inflammatory injury could be induced by cold stress in spleen tissues of quails. Furthermore, the increased expression of Hsp70 may play a role in protecting the spleen against oxidative stress and inflammatory damage caused by cold stress.

Effect of gold nanoparticles on mice splenomegaly induced by schistosomiasis mansoni.

Schistosomiasis is still one of the main parasitic diseases that affect human health in tropical regions. Whilst praziquantel (PZQ) is the main classic antischistosomal drug, the need for new drugs is still a must due to the low effectiveness of the drug on the schistosome young worms, and the evolving of PZQ resistant strains. Nanotechnology is one of the most important recent and current methods used to treat human diseases including parasitic ones. Therefore, the present study aimed to examine the curative role of gold nanoparticles (GNPs) on splenic tissue of mice infected with Schistosoma mansoni Sambon, 1907. High-resolution transmission electron microscopy was used for characterization of nanoparticles (NP). GNPs of 1 mg/kg mice body weight were inoculated into mice infected with S. mansoni. The parasite caused deteriorations in histological architecture of the spleen tissue, and splenomegaly. Additionally, the parasite induced a significant reduction in splenic tissue glutathione levels; however, the concentrations of nitric oxide and malondialdehyde were significantly increased. Treatment of mice with GNPs reduced the extent of histological impairment and oxidative stress in spleen tissue. Therefore, our results demonstrate the protective role of GNPs against splenic damage in mice infected with S. mansoni.

Anti-oxidant and anti-inflammatory effects of apigenin in a rat model of sepsis: an immunological, biochemical, and histopathological study

Objective: We hypothesize that apigenin may inhibit some cellular process of sepsis-induced spleen injury and simultaneously improve inflammation and oxidative stress. Therefore, the aim of this study was to investigate the potential protective effects of apigenin in a polymicrobial sepsis rat model of by cecal ligation and puncture.Materials and methods: 64 female Wistar albino rats were divided into 8 groups. The pro-inflammatory (tumor necrosis factor-alpha, interleukin-6, and interleukin-1-beta) and anti-inflammatory (tumor growth factor-beta and interleukin-10) cytokine levels were measured by enzyme-linked immunosorbent assay. CD3, CD68, and nuclear factor kappa B (NF-κB) positivity rates were detected by immunohistochemical methods. Oxidative stress parameters were measured by tissue biochemistry.Results: Sepsis caused a significant increase in TNF-alpha, IL-1-beta, IL-6, and TGF-beta levels whereas it reduced IL-10 level. Additionally, it led to an increase in CD3, CD68, and NF-κB positivity rates as well as oxidative stress parameters levels. However, apigenin inhibited the inflammation process, increased the IL-10 level and normalized the oxidative stress parameters.Discussion and conclusion: Pretreatment with apigenin results in a significant reduction in the amount of inflammatory cells. The beneficial effect of apigenin on spleen injury also involved inhibition of NF-κB pathway, suppression of proinflammatory cytokines, and induction of anti-inflammatory cytokine production. Additionally, it led to a decrease in oxidative stress in spleen tissue. Taking everything into account, apigenin may be an alternative therapeutic option for prevention of sepsis-induced organ.

The immunotoxic effects of short term chronic exposure to Titanium Dioxide Nanoparticles on spleen of adult albino rats and the role of after toxic effect follow up

Objective: The usage of Titanium Dioxide NanoParticles (TiO2NPs) on a large scale of applications was a reason of a variety of many health problems. The aim of the current study was to evaluate the immune toxic effects of short term administration of TiO2NPs on spleen. Material and Methods: Forty Adult male Rats were equally divided into four groups as follows: Group I: negative control, Group II: positive control, Group III: received TiO2NPs (1200 mg/kg) orally daily for 12 weeks. Group IV: follow up group received TiO2NPs by the same dose, route and for the same duration as TiO2NPs group and then they were left untreated for another 8 weeks. Total leukocytes, differential leukocytic counts, Interleukins IL-2 and IL-10 levels were measured, the spleen sections were examined immunohistochemically for the detection of CD4+ and iNOS expressing cells. Histopathological alterations in the spleen were also evaluated. Moreover, DNA damage was evaluated by comet assay. The results: TiO2NPs exposure for 12 weeks resulted in significant decreased in the total and deferential leukocytic counts, serum interleukins IL-2 as well as IL-10. It caused marked decrease in CD4+T-lymphocytes and increase in iNOS expressing cells indicating oxidative stress in spleen tissues. It also caused histopathological disruption of spleen architecture and produced DNA damage in splenocytes. Discontinuation of TiO2NPs administration for 8 weeks resulted in significant improvement of leukocytes, interleukins, increase in CD4+ T-lymphocytes and decrease in iNOS expressing cells in spleen tissues. Moreover, there was moderate improvement in histopathological alterations and DNA damage. Conclusion:TiO2NPs consumption have immunotoxic effects which may resulted from genetic damage and oxidative stress in the spleen of adult male albino rats which could be improved by its discontinuation for a period of time and it was recommended to increase the period of discontinuation as complete improvement may occur