Pub Date : 2025-08-01Epub Date: 2025-04-08DOI: 10.1080/13813455.2025.2483508
Farimah Beheshti, Mehrnoush Goudarzi, Samaneh Kakhki, S Mohammad Ahmadi-Soleimani, Mustafa Ansari, Hassan Azhdari-Zarmehri
Background: The present study conducted to assess whether vitamin D3 (Vit D) could ameliorate the anxiety and depression induced by nicotine (Nic) withdrawal in male adult rats.
Methods: To this end, behavioural tests were done in male Wistar rats undergone adolescent Nic exposure (2 mg/kg) and then withdrawal and the effect of Vit D (100, 1000, and 10,000 IU/kg) was assessed at both behavioural and biochemical levels.
Results: Results indicated that Vit D treatment could effectively prevent anxiety, depression, and biochemical alterations induced by Nic withdrawal.
Conclusion: Vit D has strong potential to be used for prevention of anxiety- and depressive-like behaviours following Nic withdrawal; however, further investigation is needed in larger sample size to discuss more confidently.
{"title":"Vitamin D<sub>3</sub> administration ameliorates the anxiety and depressive-like behaviour induced by nicotine withdrawal: a mechanistic focus on oxidative stress, inflammatory response, and serotonergic transmission.","authors":"Farimah Beheshti, Mehrnoush Goudarzi, Samaneh Kakhki, S Mohammad Ahmadi-Soleimani, Mustafa Ansari, Hassan Azhdari-Zarmehri","doi":"10.1080/13813455.2025.2483508","DOIUrl":"10.1080/13813455.2025.2483508","url":null,"abstract":"<p><strong>Background: </strong>The present study conducted to assess whether vitamin D<sub>3</sub> (Vit D) could ameliorate the anxiety and depression induced by nicotine (Nic) withdrawal in male adult rats.</p><p><strong>Methods: </strong>To this end, behavioural tests were done in male Wistar rats undergone adolescent Nic exposure (2 mg/kg) and then withdrawal and the effect of Vit D (100, 1000, and 10,000 IU/kg) was assessed at both behavioural and biochemical levels.</p><p><strong>Results: </strong>Results indicated that Vit D treatment could effectively prevent anxiety, depression, and biochemical alterations induced by Nic withdrawal.</p><p><strong>Conclusion: </strong>Vit D has strong potential to be used for prevention of anxiety- and depressive-like behaviours following Nic withdrawal; however, further investigation is needed in larger sample size to discuss more confidently.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"648-657"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-02-20DOI: 10.1080/13813455.2025.2465335
Abdulrahim Aljamal, Mahmoud Al Shawabkeh, Taha Alqadi
The aim of this study is to examine the effects of cinnamon and statins on the renal and liver functions of gentamicin-received rats.
Methods: Forty male albino rats were recruited into 4 groups (10 rat each) for a 21-day period by gavage treatment. The control group 1 was given nothing but 0.5 ml normal saline, and others injected with a dose of 100 mg/kg of Gentamicin intraperitoneally for one week before treatment. Group 2 received Gentamicin alone, Group 3 received an aqueous extract of cinnamon, and Group 4 treated with a statin medication.
Results: Gentamicin-treated group compared to other groups showed a significant increase in lever and kidney enzymes. The group treated with cinnamon or statin revealed noticeable positive effects on these markers, whereas statin showed decrease in Alanine Aminotransferase ALT levels.
Conclusion: Parameters of hepatotoxicity and nephrotoxicity induced by gentamicin were significantly reserved by cinnamon or statin, statin less effective.
{"title":"Effect of cinnamon and statins drug on kidney and liver of rats receiving gentamicin.","authors":"Abdulrahim Aljamal, Mahmoud Al Shawabkeh, Taha Alqadi","doi":"10.1080/13813455.2025.2465335","DOIUrl":"10.1080/13813455.2025.2465335","url":null,"abstract":"<p><p>The aim of this study is to examine the effects of cinnamon and statins on the renal and liver functions of gentamicin-received rats.</p><p><strong>Methods: </strong>Forty male albino rats were recruited into 4 groups (10 rat each) for a 21-day period by gavage treatment. The control group 1 was given nothing but 0.5 ml normal saline, and others injected with a dose of 100 mg/kg of Gentamicin intraperitoneally for one week before treatment. Group 2 received Gentamicin alone, Group 3 received an aqueous extract of cinnamon, and Group 4 treated with a statin medication.</p><p><strong>Results: </strong>Gentamicin-treated group compared to other groups showed a significant increase in lever and kidney enzymes. The group treated with cinnamon or statin revealed noticeable positive effects on these markers, whereas statin showed decrease in Alanine Aminotransferase ALT levels.</p><p><strong>Conclusion: </strong>Parameters of hepatotoxicity and nephrotoxicity induced by gentamicin were significantly reserved by cinnamon or statin, statin less effective.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"578-581"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-03-28DOI: 10.1080/13813455.2025.2483912
Marvellous A Acho, Ochuko L Erukainure, Veronica F Salau, Osarenkhoe O Osemwegie, Eric Amonsou, Rotimi O Arise
This study assessed the cardioprotective effects of <1 kDa peptide fractions from neem seed protein hydrolysates (NSPHs) in cardiac tissues ex vivo. Oxidative injury was induced in cardiac tissues from male Wister rats by incubating with 0.1 mM FeSO4 (pro-oxidant) for 30 minutes. Untreated tissues lacked peptide fractions, while normal control tissues lacked peptide and pro-oxidant. Treatment with the peptides increased the activities/levels of catalase, superoxide dismutase, ENTPDase, 5'NTPDase, glutathione, and HDL-cholesterol. Conversely, the levels/activities of malondialdehyde, nitric oxide, cholesterol, LDL-cholesterol, ACE, acetylcholinesterase, ATPase decreased following treatment with NSPH peptide fractions. Furthermore, the peptides depleted oxidative metabolites, while concomitantly inactivating plasmalogen synthesis and beta-oxidation of long-chain saturated fatty acids. These findings suggest that <1 kDa peptide fractions from neem seed protein hydrolysates have cardioprotective properties, potentially offering a natural therapeutic option for managing oxidative cardiac dysfunction through the regulation of oxidative stress, cholinesterase and purinergic activities, and lipid metabolism.
{"title":"Neem seed protein hydrolysates alleviate iron-induced cardiac injury via effects on angiotensin-converting enzyme, purinergic enzymes, redox balance, and lipid metabolism.","authors":"Marvellous A Acho, Ochuko L Erukainure, Veronica F Salau, Osarenkhoe O Osemwegie, Eric Amonsou, Rotimi O Arise","doi":"10.1080/13813455.2025.2483912","DOIUrl":"10.1080/13813455.2025.2483912","url":null,"abstract":"<p><p>This study assessed the cardioprotective effects of <1 kDa peptide fractions from neem seed protein hydrolysates (NSPHs) in cardiac tissues <i>ex vivo</i>. Oxidative injury was induced in cardiac tissues from male Wister rats by incubating with 0.1 mM FeSO<sub>4</sub> (pro-oxidant) for 30 minutes. Untreated tissues lacked peptide fractions, while normal control tissues lacked peptide and pro-oxidant. Treatment with the peptides increased the activities/levels of catalase, superoxide dismutase, ENTPDase, 5'NTPDase, glutathione, and HDL-cholesterol. Conversely, the levels/activities of malondialdehyde, nitric oxide, cholesterol, LDL-cholesterol, ACE, acetylcholinesterase, ATPase decreased following treatment with NSPH peptide fractions. Furthermore, the peptides depleted oxidative metabolites, while concomitantly inactivating plasmalogen synthesis and beta-oxidation of long-chain saturated fatty acids. These findings suggest that <1 kDa peptide fractions from neem seed protein hydrolysates have cardioprotective properties, potentially offering a natural therapeutic option for managing oxidative cardiac dysfunction through the regulation of oxidative stress, cholinesterase and purinergic activities, and lipid metabolism.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"670-682"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143727486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-09DOI: 10.1080/13813455.2025.2489721
Zhiping Huang, Chaoqian Liu, Xiang Zhao, Yan Guo
Purpose: Bariatric surgery can effectively alleviate obesity and diabetes by regulation of the gut microbiota. This study aimed to investigate the change in the gut microbiota metabolite TMAO and to explore its effect on glucose metabolism after sleeve gastrectomy (SG).
Materials and methods: Diet-induced obesity mouse models were established, and the mice were randomly divided into four groups: an SG group, a sham-operated group pair-fed with the SG group (PF), a sham-operated group fed ad libitum (AL), and a lean control group (C). At 10 weeks post-surgery, the changes in glycogen content of liver, gut microbiota and the level of FMO3 in the liver were evaluated, and their correlation with TMAO production was analysed. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured.
Results: At 10 weeks post-surgery, hepatocyte glycogen levels were restored, and serum TMA and TMAO levels were significantly increased. Faecal metagenomic sequencing results showed that the abundances of Ruminococcaceae and Lachnospiraceae, which were positively correlated with TMAO production, were significantly increased after surgery. While the changes in FMO3, the key enzyme producing TMAO in the liver was found decreased significantly after SG. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured. Inconsistent with the changing trend of TMAO, the expression of PERK, FOXO1, PCK, and G6PC significantly decreased after SG.
Conclusions: SG can significantly reduce obesity and restore glucose metabolism. After surgery, TMAO metabolites increased in a microbiota-dependent manner.
{"title":"The effect of elevated levels of the gut metabolite TMAO on glucose metabolism after sleeve gastrectomy.","authors":"Zhiping Huang, Chaoqian Liu, Xiang Zhao, Yan Guo","doi":"10.1080/13813455.2025.2489721","DOIUrl":"10.1080/13813455.2025.2489721","url":null,"abstract":"<p><strong>Purpose: </strong>Bariatric surgery can effectively alleviate obesity and diabetes by regulation of the gut microbiota. This study aimed to investigate the change in the gut microbiota metabolite TMAO and to explore its effect on glucose metabolism after sleeve gastrectomy (SG).</p><p><strong>Materials and methods: </strong>Diet-induced obesity mouse models were established, and the mice were randomly divided into four groups: an SG group, a sham-operated group pair-fed with the SG group (PF), a sham-operated group fed ad libitum (AL), and a lean control group (C). At 10 weeks post-surgery, the changes in glycogen content of liver, gut microbiota and the level of FMO3 in the liver were evaluated, and their correlation with TMAO production was analysed. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured.</p><p><strong>Results: </strong>At 10 weeks post-surgery, hepatocyte glycogen levels were restored, and serum TMA and TMAO levels were significantly increased. Faecal metagenomic sequencing results showed that the abundances of Ruminococcaceae and Lachnospiraceae, which were positively correlated with TMAO production, were significantly increased after surgery. While the changes in FMO3, the key enzyme producing TMAO in the liver was found decreased significantly after SG. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured. Inconsistent with the changing trend of TMAO, the expression of PERK, FOXO1, PCK, and G6PC significantly decreased after SG.</p><p><strong>Conclusions: </strong>SG can significantly reduce obesity and restore glucose metabolism. After surgery, TMAO metabolites increased in a microbiota-dependent manner.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"691-700"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-03-02DOI: 10.1080/13813455.2025.2465337
Qian Zhang, Yan Huo, Runying Zhu, Xujie Zhang, Lingwei Zeng, Zhenjie Hu
Objective: This study explores the mechanism of methyltransferase like 3 (METTL3) on sepsis-associated encephalopathy (SAE)-induced hippocampal neuronal injury.
Methods: A murine model of SAE was established by caecal ligation and puncture. Hippocampal cells were induced by lipopolysaccharide (LPS). The mouse survival was observed and behavioural tests evaluated cognitive function. METTL3 and glutamic-oxaloacetic transaminase 1 (GOT1) expressions were detected via RT-qPCR and Western blot. Immunofluorescence staining examined the co-localization of NeuN and METTL3. The m6A enrichment on GOT1 was determined by MeRIP.
Results: METTL3 and GOT1 were highly expressed in SAE mice and LPS-stimulated hippocampal cells. SAE mice exhibited cognitive function impairment, reduced survival rate, and decreased neuronal cells. LPS induction increased hippocampal cell apoptosis and enhanced inflammation. Silence of METTL3 reduced hippocampal neuronal injury in SAE mice and LPS-induced hippocampal cell injury.
{"title":"Molecular mechanism of METTL3 regulating hippocampal neuronal injury induced by sepsis-associated encephalopathy.","authors":"Qian Zhang, Yan Huo, Runying Zhu, Xujie Zhang, Lingwei Zeng, Zhenjie Hu","doi":"10.1080/13813455.2025.2465337","DOIUrl":"10.1080/13813455.2025.2465337","url":null,"abstract":"<p><strong>Objective: </strong>This study explores the mechanism of methyltransferase like 3 (METTL3) on sepsis-associated encephalopathy (SAE)-induced hippocampal neuronal injury.</p><p><strong>Methods: </strong>A murine model of SAE was established by caecal ligation and puncture. Hippocampal cells were induced by lipopolysaccharide (LPS). The mouse survival was observed and behavioural tests evaluated cognitive function. METTL3 and glutamic-oxaloacetic transaminase 1 (GOT1) expressions were detected via RT-qPCR and Western blot. Immunofluorescence staining examined the co-localization of NeuN and METTL3. The m6A enrichment on GOT1 was determined by MeRIP.</p><p><strong>Results: </strong>METTL3 and GOT1 were highly expressed in SAE mice and LPS-stimulated hippocampal cells. SAE mice exhibited cognitive function impairment, reduced survival rate, and decreased neuronal cells. LPS induction increased hippocampal cell apoptosis and enhanced inflammation. Silence of METTL3 reduced hippocampal neuronal injury in SAE mice and LPS-induced hippocampal cell injury.</p><p><strong>Conclusion: </strong>METTL3-mediated m6A modification on GOT1 mRNA elevates GOT1 expression, thereby aggravating SAE-induced hippocampal neuronal injury.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"582-592"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-02-21DOI: 10.1080/13813455.2025.2456876
Yujie Zhang, Yi Ye, Xiaorui Jia, Pu Wang, Zheng Xiong, Hui Zhu
Gestational diabetes mellitus (GDM) is one of the most prevalent metabolic diseases in pregnant women. In this study, we investigated the effects of Salusin-α in rodent models of GDM. We observed decreased levels of Salusin-α in the placental tissue of GDM mice. Salusin-α alleviated GDM symptoms by reducing blood glucose and increasing serum insulin levels. Further analysis revealed that Salusin-α improved lipid profiles and foetal outcomes in GDM mice. Additionally, Salusin-α mitigated oxidative and nitrosative stress in the placental tissue of GDM mice by enhancing the levels of Vitamin E, Vitamin C, and reduced GSH, while decreasing levels of TBARS and nitric oxide metabolites (nitrite + nitrate = NOx). Salusin-α also reduced the levels of MCP-1 and IL-8. Mechanically, Salusin-α inhibited the activation of p38/NF-κB by reducing phosphorylated p38 and phosphorylated NF-κB p65. In conclusion, our findings support the potential clinical application of Salusin-α as a novel peptide for molecular intervention in GDM.
{"title":"The protective effects of Salusin-α against oxidative stress and inflammatory response in mice with gestational diabetes mellitus (GDM).","authors":"Yujie Zhang, Yi Ye, Xiaorui Jia, Pu Wang, Zheng Xiong, Hui Zhu","doi":"10.1080/13813455.2025.2456876","DOIUrl":"10.1080/13813455.2025.2456876","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) is one of the most prevalent metabolic diseases in pregnant women. In this study, we investigated the effects of Salusin-α in rodent models of GDM. We observed decreased levels of Salusin-α in the placental tissue of GDM mice. Salusin-α alleviated GDM symptoms by reducing blood glucose and increasing serum insulin levels. Further analysis revealed that Salusin-α improved lipid profiles and foetal outcomes in GDM mice. Additionally, Salusin-α mitigated oxidative and nitrosative stress in the placental tissue of GDM mice by enhancing the levels of Vitamin E, Vitamin C, and reduced GSH, while decreasing levels of TBARS and nitric oxide metabolites (nitrite + nitrate = NOx). Salusin-α also reduced the levels of MCP-1 and IL-8. Mechanically, Salusin-α inhibited the activation of p38/NF-κB by reducing phosphorylated p38 and phosphorylated NF-κB p65. In conclusion, our findings support the potential clinical application of Salusin-α as a novel peptide for molecular intervention in GDM.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"493-502"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143472082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-11-23DOI: 10.1080/13813455.2024.2432763
{"title":"Correction.","authors":"","doi":"10.1080/13813455.2024.2432763","DOIUrl":"10.1080/13813455.2024.2432763","url":null,"abstract":"","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"567"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-02-03DOI: 10.1080/13813455.2025.2459283
Hamed Alizadeh Pahlavani, Ali Veisi
Objective: Androgenic steroids abuse among young athletes has long-term health consequences, causing profound damage to vital organs such as the heart, blood vessels, brain, liver, gonads, kidneys, and skin.
Results: In the vessels, steroids cause plaque formation, vascular calcification, thrombosis, and coronary artery disease, and in the heart, they lead to pathological fibrosis, dilated cardiomyopathy, heart failure, fatal ventricular arrhythmias, acute myocardial infarction, and reduced ejection fraction. The brain also suffers from cognitive decline, memory impairment, and a constellation of neurotransmitter abnormalities that lead to depression. In the liver, the consequences are severe and manifest as increased oxidative stress, liver dysfunction, hepatotoxicity, cholestatic jaundice, liver tumours, cell death, and elevations in liver enzymes, bilirubin, and cholesterol. Male athletes experience testicular atrophy, temporary suppression of spermatogenesis, hypogonadism, reduced fertility, infertility, and hormonal imbalance. In contrast, women experience ovarian dysfunction and menstrual irregularities. In the kidney, steroids lead to increased inflammatory cytokines, fibrosis, renal tubular hypertrophy, glomerular changes, and structural damage, and show higher levels of serum creatinine, urinary protein, and cystatin C. In athletes, steroids can lead to various skin problems such as acne, gynecomastia, prostatitis, and alopecia.
{"title":"Possible consequences of the abuse of anabolic steroids on different organs of athletes.","authors":"Hamed Alizadeh Pahlavani, Ali Veisi","doi":"10.1080/13813455.2025.2459283","DOIUrl":"10.1080/13813455.2025.2459283","url":null,"abstract":"<p><p><b>Objective:</b> Androgenic steroids abuse among young athletes has long-term health consequences, causing profound damage to vital organs such as the heart, blood vessels, brain, liver, gonads, kidneys, and skin.</p><p><p><b>Results:</b> In the vessels, steroids cause plaque formation, vascular calcification, thrombosis, and coronary artery disease, and in the heart, they lead to pathological fibrosis, dilated cardiomyopathy, heart failure, fatal ventricular arrhythmias, acute myocardial infarction, and reduced ejection fraction. The brain also suffers from cognitive decline, memory impairment, and a constellation of neurotransmitter abnormalities that lead to depression. In the liver, the consequences are severe and manifest as increased oxidative stress, liver dysfunction, hepatotoxicity, cholestatic jaundice, liver tumours, cell death, and elevations in liver enzymes, bilirubin, and cholesterol. Male athletes experience testicular atrophy, temporary suppression of spermatogenesis, hypogonadism, reduced fertility, infertility, and hormonal imbalance. In contrast, women experience ovarian dysfunction and menstrual irregularities. In the kidney, steroids lead to increased inflammatory cytokines, fibrosis, renal tubular hypertrophy, glomerular changes, and structural damage, and show higher levels of serum creatinine, urinary protein, and cystatin C. In athletes, steroids can lead to various skin problems such as acne, gynecomastia, prostatitis, and alopecia.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"393-409"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-11-16DOI: 10.1080/13813455.2024.2426497
Bartholomew I C Brai, Ruth Ometere Joseph, Titilope Ruth Komolafe, Busayo Elizabeth Amosun, Olamide Olajusi Crown, Kayode Komolafe, Ifedayo Victor Ogungbe
The neem plant (Azadirachta indica) has popular ethnomedicinal applications. The anti-diabetic potential and mechanism of neem seed oil (NSO) in a rodent model of type 2 diabetes mellitus was evaluated in the present study. Experimentally-induced diabetic animals were administered NSO (200 and 400 mg/kg) or metformin (150 mg/kg) orally for 30 days, with some animals serving as positive and negative controls. NSO significantly (p < .05) reversed diabetes-induced impaired glucose metabolism, dyslipidaemia, and oxido-inflammatory imbalances typified by changes in the NADH/NAD+ ratio (p < .001) and increases in the mRNA or protein levels of C-reactive protein, 4-hydroxynonenal, and pro-inflammatory cytokines (TNF-α and Il-1β) among others in the hepatic or pancreatic tissues of diabetic animals. The histological evaluation of the pancreatic tissue corroborated the protective effect of NSO. The findings showed that the antidiabetic effect of NSO proceeded through its hypolipidemic effect and modulation of redox and inflammatory signalling events in the tissues of animals.
{"title":"Neem seed oil ameliorates diabetic phenotype by suppressing redox imbalance, dyslipidaemia and pro-inflammatory mediators in a rodent model of type 2 diabetes.","authors":"Bartholomew I C Brai, Ruth Ometere Joseph, Titilope Ruth Komolafe, Busayo Elizabeth Amosun, Olamide Olajusi Crown, Kayode Komolafe, Ifedayo Victor Ogungbe","doi":"10.1080/13813455.2024.2426497","DOIUrl":"10.1080/13813455.2024.2426497","url":null,"abstract":"<p><p>The neem plant (<i>Azadirachta indica</i>) has popular ethnomedicinal applications. The anti-diabetic potential and mechanism of neem seed oil (NSO) in a rodent model of type 2 diabetes mellitus was evaluated in the present study. Experimentally-induced diabetic animals were administered NSO (200 and 400 mg/kg) or metformin (150 mg/kg) orally for 30 days, with some animals serving as positive and negative controls. NSO significantly (<i>p</i> < .05) reversed diabetes-induced impaired glucose metabolism, dyslipidaemia, and oxido-inflammatory imbalances typified by changes in the NADH/NAD+ ratio (<i>p</i> < .001) and increases in the mRNA or protein levels of C-reactive protein, 4-hydroxynonenal, and pro-inflammatory cytokines (TNF-α and Il-1β) among others in the hepatic or pancreatic tissues of diabetic animals. The histological evaluation of the pancreatic tissue corroborated the protective effect of NSO. The findings showed that the antidiabetic effect of NSO proceeded through its hypolipidemic effect and modulation of redox and inflammatory signalling events in the tissues of animals.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"351-365"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-12-30DOI: 10.1080/13813455.2024.2447532
Yan Hui, Yuyang Dong, Yi Liu
Diabetic nephropathy (DN) is the main cause of end-stage kidney disease and has become a global public health problem. Currently, treatment of DN is limited to alleviating disease progression rather than curing diseases or restoring renal function, thus more effective therapeutic strategies against DN are urgently needed. Mesenchymal stem cells (MSCs) have been widely applied in the prevention and treatment of DN. Preclinical studies have proved that MSCs exhibited favourable therapeutic effects on DN by regulation of hyperglycaemia, reduction of urinary albumin, and protecting renal function. Hence this review provides an overview of the biological properties of MSCs, summarises the regulatory mechanisms of MSC-based therapy for DN, presents ongoing or completed clinical trials, as well as discusses the potential challenges and new strategies of MSCs in the treatment of DN, with the aim of providing a balanced and unbiased view of MSC transplantation as promising therapeutic strategies for DN.
{"title":"Research advance in mesenchymal stem cell-based therapy for diabetic nephropathy.","authors":"Yan Hui, Yuyang Dong, Yi Liu","doi":"10.1080/13813455.2024.2447532","DOIUrl":"https://doi.org/10.1080/13813455.2024.2447532","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is the main cause of end-stage kidney disease and has become a global public health problem. Currently, treatment of DN is limited to alleviating disease progression rather than curing diseases or restoring renal function, thus more effective therapeutic strategies against DN are urgently needed. Mesenchymal stem cells (MSCs) have been widely applied in the prevention and treatment of DN. Preclinical studies have proved that MSCs exhibited favourable therapeutic effects on DN by regulation of hyperglycaemia, reduction of urinary albumin, and protecting renal function. Hence this review provides an overview of the biological properties of MSCs, summarises the regulatory mechanisms of MSC-based therapy for DN, presents ongoing or completed clinical trials, as well as discusses the potential challenges and new strategies of MSCs in the treatment of DN, with the aim of providing a balanced and unbiased view of MSC transplantation as promising therapeutic strategies for DN.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":"131 3","pages":"379-392"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}