Prospective Antiviral Effect of Ulva lactuca Aqueous Extract against COVID-19 Infection.

Marine algal extracts exhibit a potent inhibitory effect against several enveloped and non-enveloped viruses. The infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has several adverse effects, including an increased mortality rate. The anti-COVID-19 agents are still limited; this issue requires exploring novel, effective anti-SARS-CoV-2 therapeutic approaches. This study investigated the antiviral activity of an aqueous extract of Ulva lactuca, which was collected from the Gulf of Suez, Egypt. The aqueous extract of Ulva lactuca was characterized by high-performance liquid chromatography (HPLC), Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), and Energy Dispersive X-ray (EDX) analyses. According to the HPLC analysis, the extract comprises several sugars, mostly rhamnose (32.88%). The FTIR spectra showed numerous bands related to the functional groups. EDX analysis confirmed the presence of different elements, such as oxygen (O), carbon (C), sulfur (S), magnesium (Mg), potassium (K), calcium (Ca), and sodium (Na), with different concentrations. The aqueous extract of U. lactuca (0.0312 mg/mL) exhibited potent anti-SARS-CoV-2 activity via virucidal activity, inhibition of viral replication, and interference with viral adsorption (% inhibitions of 64%, 33.3%, and 31.1%, respectively). Consequently, ulvan could be a promising compound for preclinical study in the drug development process to combat SARS-CoV-2.

Correction: Neamatallah et al. Nano Ellagic Acid Counteracts Cisplatin-Induced Upregulation in OAT1 and OAT3: A Possible Nephroprotection Mechanism. Molecules 2020, 25, 3031.

In the original publication, there was a mistake in Figure 3 as published [...].

Apocynin attenuates methotrexate-induced mucositis by regulating NF-κB, PPAR-γ and Bax/Bcl-2/Puma signals.

Oxidative stress, inflammation and apoptosis are the primary inducers of Methotrexate (MTX)-induced mucositis. This research aimed to determine whether apocynin (APO) could protect against MTX-induced mucositis. The antioxidants, anti-inflammatory and anti-apoptotic actions of APO in this model will be evaluated. The experiment was performed on 32 rats. A single dose (20 mg/kg) of MTX was injected i.p. to induce intestinal mucositis. APO was given orally once per day at a dose of 100mg/kg (five days prior to and five days following an MTX injection). APO safeguarded the histological structure of the duodenal mucosa, as observed by the conserved histology of goblet cells (villi and crypts). APO mitigated oxidative stress by reducing intestin MDA and raising GSH, SOD and GST, also suppressing NF-κB mRNA expression. Intestinal content of proinflammatory cytokines was reduced in APO-treated MTX rats, with downregulation of proinflammatory iNOS and upregulation of anti-inflammatory PPAR-γ proteins. The intestinal mucosa of rats treated with APO and MTX displayed weekly positive immune staining for cleaved caspase-3. APO upregulate the anti-apoptotic Bcl2 mRNA and down regulate the proapoptotic Bax and Puma mRNA in the duodenal mucosa. The results indicate the possibility of using APO as a novel therapeutic agent to prevent MTX-induced mucositis.

Elevated Salivary Inflammatory Biomarkers are Associated with SARS-CoV-2 Infection Severity.

High levels of inflammatory cytokines in serum have been reported in patients with severe SARS-CoV-2 infection. There is growing interest in recognizing the role of inflammatory biomarkers in saliva in diagnosing systemic diseases. This study assumed that estimating biomarkers in saliva samples from patients infected with SARS-CoV-2 would distinguish between mild and severe cases. Saliva was collected from 142 controls and 158 SARS-CoV-2 patients (mild 72 and severe 86) to measure interleukin-6 (IL-6), C-reactive protein (CRP), and C-X-C motif chemokine ligand-10 (CXCL-10). IL-6 and CXCL-10 were significantly increased in patients with mild and severe SARS-CoV-2 infections. CRP was significantly increased only in severe SARS-CoV-2 cases. All biomarkers were significantly higher in severe cases than in mild cases (p < 0.001). Among patients with SARS-CoV-2 infection, men showed significantly higher CRP and CXCL-10 levels than females (p < 0.01 and 0.05, respectively). In addition, elderly patients (40-80 years) had significantly higher IL-6, CRP, and CXCL-10 (p < 0.001). Patients with diabetes and hypertension showed elevated IL-6, CRP, and CXCL-10 (p < 0.001). There was a significant positive correlation between IL-6, CRP, CXCL-10, and between age, IL-6, CRP, and CXCL-10. Saliva may have a future value in measuring the inflammatory biomarkers associated with the severity of SARS-CoV2 infection and therapeutic monitoring.

Effect of prolonged whole-body hyperthermia on adult male rat testes and the protective role of vitamin C and E: A histological and biochemical study.

Hyperthermia (HT) is a significant risk factor for male infertility. Most researchers investigated the effect of localized and short-term HT on male fertility. This study aimed to assess the harmful impacts of prolonged and generalized HT on testicular histology and ultrastructure in rats. The possible protective effects of vitamin E (Vit E), Vit C, and their combination were also investigated. Thirty male adult Wister rats were used (5 groups). 1- control, 2- HT, 3- Vit C, 4- Vit E, and 5- Vit C + Vit E. Rats in groups 2-5 were subjected to HT (41°C), 1 hr daily for 2 weeks. HT-induced a significant decrease in body weight gain, food and water intake, and serum testosterone. HT showed a damaging effect on the testicular and coda epididymis tissue. HT significantly (p ≤ .05) produced oxidative stress (decreased serum catalase (145.49 ± 8.98), glutathione peroxidase (20.27 ± 4.46), superoxide dismutase (2.68 ± 0.54), and reduced glutathione (5.18 ± 0.33), and increased malondialdehyde (9.46 ± 1.55). Vit E alone and combined with Vit C, significantly protected the gonads against the deleterious effects of HT. The results recommended that prolonged HT of the whole body is harmful to male fertility. Prophylactic therapy with Vit E could help decrease the HT-induced male gonadal harm.

Trimetazidine improved adriamycin-induced cardiomyopathy by downregulating TNF-α, BAX, and VEGF immunoexpression via an antioxidant mechanism.

Few studies have reported a prophylactic effect of the anti-ischemic trimetazidine (TRI) against cardiac toxicity caused by adriamycin (ADR). However, the mechanism of action of TRI remained incomplete. The cardioprotective mechanism(s) of TRI against ADR-induced cardiotoxicity was investigated in this study. Cardiotoxicity was induced in three groups of Wistar rats by injecting a single dose of ADR (10 mg/kg, i.p.). TRI was administered in two doses regimen, low (L) (2.5 mg/kg, i.p.) and high (H) (10 mg/kg, i.p.). The results of the study showed that both TRI L and H doses improved cardiac enzymes and pathology, while only the TRI H dose improved the electrocardiogram. Both TRI L and H doses decreased malondialdehyde and increased reduced glutathione and superoxide dismutase. Only TRI H dose increased glutathione peroxidase and catalase. Both TRI L and H doses decreased interleukin-1 beta and tumor necrosis factor-alpha (TNF-α). Both TRI L and H doses downregulated TNF-α, BAX, and vascular endothelial growth factor cardiac protein expression. The data obtained in this study provided evidence that TRI opposed ADR-induced cardiotoxicity. The mechanism could be due to improved antioxidant levels as well as inhibition of inflammation and programmed cell death.

Colon-Targeted Therapy of Tacrolimus (FK506) in the Treatment of Experimentally Induced Colitis.

BACKGROUND/AIMS: Inflammatory bowel disease is a chronic or remitting/relapsing intestinal inflammation, which comprises Crohn's disease and ulcerative colitis (UC). Severe UC is a life-threatening condition that requires corticosteroids (CS) as a first-line rescue therapy. Some patients are refractory to CS and may require alternative immunosuppressive therapy. Oral tacrolimus (FK506), an immunosuppressive agent, has been reported to be effective in the management of severe refractory UC, but it can cause serious adverse effects. This work aims to study the effect of tacrolimus delivered by a colon-targeted delivery system (CTDS) in a dextran sulfate sodium (DSS)-induced animal model of colitis. MATERIALS AND METHODS: We developed and evaluated an oral CTDS of tacrolimus (FK506) loaded pH-dependent polymeric microspheres, composed of Eudragit® S100 as a pH-sensitive polymer using the oil-in-water emulsion method. The physicochemical properties and drug release profiles of these microparticles in gastrointestinal tract (GIT) conditions were examined. A DSS-induced colitis rat model was used to evaluate the potential remedial and in vivo distribution of microspheres. RESULTS: The pH-microspheres prevented a burst drug release in acidic pH conditions and showed sustained release at a colonic pH. The in vivo distribution study in the rat GIT demonstrated that pH-microspheres were successfully delivered to the inflamed colon. Moreover, it also demonstrated a significant decrease of disease activity and expression of proinflammatory cytokines, such as tumor necrosis factor α, interleukin-1ß (IL-1ß), and IL-6, and minimized the histological and morphometric changes. CONCLUSION: The results confirmed the efficacy of tacrolimus (FK506) CTDs in the management of DSS-induced colitis.

Nano Ellagic Acid Counteracts Cisplatin-Induced Upregulation in OAT1 and OAT3: A Possible Nephroprotection Mechanism.

Cisplatin is an anticancer drug commonly used for solid tumors. However, it causes nephrotoxicity. OAT1 and OAT3 are organic anion transporters known to contribute to the uptake of cisplatin into renal tubular cells. The present study was designed to examine the protective role of ellagic acid nanoformulation (ellagic acid nano) on cisplatin-induced nephrotoxicity in rats, and the role of OAT1/OAT3 in this effect. Four groups of male Wistar rats were used (n = 6): (1) control, (2) cisplatin (7.5 mg/kg single dose, intraperitoneal), (3) cisplatin + ellagic acid nano (1 mg/kg), and (4) cisplatin + ellagic acid nano (2 mg/kg). Nephrotoxic rats treated with ellagic acid nano exhibited a significant reduction in elevated serum creatinine, urea, and oxidative stress marker, malondialdehyde (MDA). Additionally, ellagic acid nano restored renal glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Ellagic acid nano improved the histopathological changes induced by cisplatin, such as tubular dilatation, necrosis, and degeneration. Interestingly, OAT1 and OAT3 showed significantly lower expression at both mRNA and protein levels following ellagic acid nano treatment relative to the cisplatin-exposed group. These findings reveal a potential inhibitory role of ellagic acid antioxidant on OAT1 and OAT3 expression and thus explains its nephroprotective effect against cisplatin nephrotoxicity.

Biochemical and histological evidence of thyroid gland dysfunction in estradiol valerate model of the polycystic ovary in Wistar rats.

Thyroid defects and polycystic ovary (PSO) disease are prevalent endocrine problems among humans. While various studies investigated the ovarian function and histological alterations during estradiol valerate model of PCO, yet, there were no available studies examining thyroid gland function and histology. Therefore, the present study aimed to investigate linkage between estradiol valerate-induced PCO and the development of thyroid dysfunction in rats. The study comprises 2 groups of male Wistar rats (n = 12), control group and PCO group. PCO was induced by injecting two doses of estradiol valerate with 6 weeks lag period in between. After twelve weeks, PCO was confirmed by vaginal smear examination which showed marked vaginal cornification. In addition, the light microscopic examination of the ovaries revealed chief histological signs of PCO like numerous cysts and damaged follicles. In addition, PCO-induced rats showed decreased serum LH and increased serum FSH levels. Thyroid hypoactivity was confirmed by increased serum TSH and decreased serum thyroid hormones (T3, and T4). Histologically, the thyroid tissue revealed small-size follicles devoid of the colloid and increased connective tissue between follicles. Semithin sections showed hypertrophied and/or flat follicular cells as well as increased resorption colloidal granules. Ultrathin sections showed low height cells with dark nucleus and heterochromatin. Furthermore, PCO-induced rats thyroid gland tissue revealed increased expression of the apoptotic mediator caspase-3. There was also a decrease in the expression of proliferating cell nuclear antigen. In summary, this study provides several effective biochemical and histological evidences for thyroid gland dysfunction in PCO-induced rats.

Proanthocyanidin protects against cisplatin-induced oxidative liver damage through inhibition of inflammation and NF-κß/TLR-4 pathway.

Although cisplatin (CIS) is a highly effective anticancer drug, hepatotoxicity is one of the most common adverse effects associated with its use. Recently, reactive oxygen species (ROS) and inflammation are suggested to be key factors in the pathophysiology of CIS-induced acute liver damage. The aim of this study is to investigate the possible protective effect of proanthocyanidin (PRO) against CIS-induced acute hepatotoxicity. Rats were divided into four groups: 1, Control; 2, PRO; 3, CIS; and 4, PRO + CIS. Biochemical studies and histopathology were used to assess liver damage. ROS, inflammatory cytokines, nuclear factor kappa beta (NF-κß), inducible cyclooxygenase enzyme (COX-2), inducible nitric oxide synthase (iNOS), toll-like receptor-4 (TLR-4) gene expression, and apoptotic markers were also assessed. PRO pretreatment protected the liver against CIS-induced toxicity as indicated by decreased plasma levels of liver function enzymes and the normal liver histopathology observed in the PRO + CIS group. PRO pretreatment also diminished indicators of oxidative stress in the liver, including nitric oxide (NO) and malondialdehyde (MDA). It also increased the antioxidants, reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) in the liver. Plasma interleukin-1 beta (IL-1ß), IL-6, and tumor necrosis factor-alpha (TNF-α) were all reduced. Liver gene expression of NF-κß, COX-2, iNOS, and TLR-4 were all downregulated. Furthermore, PRO administration downregulated the liver expression of the apoptotic marker, Bax, while upregulated the antiapoptotic marker, Bcl2. In conclusion, our results revealed that PRO may protect against CIS-induced acute liver damage mainly through inhibition of ROS, inflammation, and apoptosis.

Ameliorative effect of lycopene against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced rat liver microsomal toxicity: an in vitro study.

The objective of the current study was to investigate the potential oxidative damage of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in hepatic microsomal fractions in vitro and to further elucidate the potential modulatory effect of lycopene. Rat liver microsomes were divided into four groups. Group I served as a control and is incubated with vehicle (toluene). Groups II and IV were incubated with 20 µM lycopene for 1 h before further incubating; groups III and IV with 15 nM of TCDD for further 1 h. Hydrogen peroxide (H2O2) production, lipid peroxidation (LPO), protein carbonyl content and activities of uridine 5'-diphospho-glucuronyltransferase (UDPGT) and P450 were significantly increased. Moreover, the activity of antioxidant enzymes superoxide dismutase, glutathione peroxidase, catalse, glutathione-S-transferase and glutathione reductase as well as the microsomal thiol content were significantly decreased. Incubation with lycopene (group IV) maintained near normal activities of the enzymes, normalized thiol and carbonyl content and significantly reduced LPO and H2O2 production. In conclusion, the findings of the study indicate that TCDD induces a significant oxidative stress in liver microsomes as manifested by increased LPO, H2O2 production, protein carbonyl content and activities of UDPGT and P450 and decreased antioxidant enzymes activities and thiol content. By the reversal of biochemical and oxidative markers toward normalcy, the protective role of lycopene is illuminated in rat liver microsomal toxicity.

Cilostazol protects against gastric ulcers by regulating PPAR-γ, HO-1, PECAM-1, pErk-1, NF-κB, Bcl-2, and cleaved caspase-3 protein expression.

Millions of individuals worldwide, across all age groups, suffer from the widespread health issue of gastric ulcers. In many experiments, cilostazol (Cls), a phosphodiesterase-3 inhibitor, was recently shown to have anti-ulcer activity. Notably, Cls increases the expression and transcriptional activity of PPAR-γ in vitro and in vivo. This study aimed to evaluate the protective effect of Cls against ethanol-induced gastric ulcers and clarify the possible underlying mechanisms with an emphasis on the role of PPAR-γ. Male albino rats were treated with ethanol to induce gastric ulcers, or they were pretreated with Cls, omeprazole (Omp), GW9662, or Cls + GW9662 for 14 consecutive days before receiving ethanol. Cls protects against ethanol-induced gastric ulcers. Cls treatment significantly reduced ethanol-induced upregulation of the pro-inflammatory markers (IL-1ß, IL-6, TNF-α, and NF-κB), MDA (a marker of lipid peroxidation), and caspase-3 and cleaved caspase-3 (apoptotic markers). On the other hand, Cls treatment counteracted ethanol-induced downregulation of PPAR-γ, pErk-1, HO-1 and GSH (antioxidant markers), PECAM-1 and NO (healing markers), and Bcl-2 (antiapoptotic marker). However, when combined with GW9662, a potent antagonist of PPAR-γ, Cls loses its effects. In conclusion, these results suggest that PPAR-γ and pErk-1 are essential for Cls's protective effects against ethanol-induced gastric ulcers.

The emerging role of α7nAChRs/caspase-3/Nrf-2 signaling pathway in citicoline improved autistic behavior induced by thimerosal in mice.

AIMS: Autism spectrum disorder (ASD) is a global concern,affecting around 75 million individuals.Various factors contribute to ASD,including mercury-containing preservatives like thimerosal (Thim) found in some vaccines.This study explored whether citicoline could be a therapeutic option for Thim-induced neuronal damage in a mouse model of ASD.Additionally,the study investigated the effects of citicoline on the α7nAChRs/Akt/Nrf2/caspase-3 pathway,which may be involved in the development of ASD. MATERIALS AND METHODS: The study separated newborn mice into four groups.The control group received saline injections,while the Thim group received intramuscular injections of 3000 µg Hg/kg Thim on days 7,9,11,and 15 after birth.The two citicoline groups were administered Thim followed by intraperitoneal injections of 250 mg/kg or 500 mg/kg citicoline for three weeks.Afterward,various parameters were assessed, including growth,behavior,brain histopathology,oxidative stress,apoptotic,and inflammatory markers. KEY FINDINGS: Untreated Thim-exposed mice exhibited significant brain damage,which was substantially alleviated by citicoline treatment.This beneficial effect was associated with increased expressions and concentrations of brain α7nAChRs and Akt, increased brain content of Nrf2, and the hippocampus contents of acetylcholine. Citicoline treatment decreased the brain levels of oxidative stress markers (MDA and NO),the apoptotic marker caspase-3,and pro-inflammatory markers (NF-κB,TNF-α,and IL-1ß). The drug also increased the brain GPx activity. SIGNIFICANCE: Based on the results of this study,the α7nAChRs pathway appears to be essential for the therapeutic effectiveness of citicoline in treating Thim-induced ASD in mice.

Protective role of naftidrofuryl against methotrexate-induced testicular damage via the amelioration of the p53/miRNA-29a/CDC42 apoptotic pathway, inflammation, and oxidative stress.

This study aimed to assess the possible protective effects of naftidrofuryl (Naf) against methotrexate (MTX)-induced testicular toxicity in rats. Male rats were randomly distributed into four groups: control, Naf, MTX, and MTX+Naf groups. MTX administration induced oxidative stress, inflammation, and apoptosis in the testicular tissue, while pretreatment with Naf attenuated these pathways. Naf pretreatment significantly decreased malondialdehyde and interleukin-6 contents, microRNA-29a (miRNA-29a) expression level, and nuclear factor kappa B and p53 immunostaining in the testicular tissues compared to the MTX group. Conversely, it significantly increased Johnsen's score, serum testosterone level, serum total antioxidant capacity, testicular superoxide dismutase activity, testicular catalase activity, and testicular cell division cycle 42 (CDC42) expression compared to the MTX group. In conclusion, Naf exerted a significant protective effect against MTX-induced testicular toxicity via antioxidant and anti-inflammatory mechanisms and modulating the p53/miRNA-29a/CDC42 apoptotic pathway.

Protective effect of carvedilol on adriamycin-induced left ventricular dysfunction in children with acute lymphoblastic leukemia.

BACKGROUND: Adriamycin (ADR) is a potent chemotherapeutic agent widely used in the treatment of childhood acute lymphoblastic leukemia (ALL); its clinical use is limited owing to its marked cardiotoxicity. The present study investigated the possible protective role of carvedilol on ADR-induced left ventricular dysfunction in children with ALL. METHODS AND RESULTS: Fifty children with newly diagnosed ALL were included in this study. They were divided into 2 equal groups: 1) ADR; and 2) ADR + carvedilol. Patients were evaluated with conventional 2-dimensional echocardiographic examination (2D), pulsed tissue Doppler (PTD), and 2-dimensional longitudinal strain echocardiography (2DS) before and after therapy. Plasma lactic dehydrogenase (LDH), creatine phosphokinase (CPK), and troponin I levels were also determined before and after therapy. ADR treatment reduced left ventricular systolic dysfunction as assessed by a significant decrease in fractional shortening (FS) (2D) and global peak-systolic strain (GPSS; 2DS). In addition, ADR treatment significantly increased plasma troponin I and LDH. Pretreatment of ADR-treated patients with carvedilol resulted in a significant increase in FS (2D) and GPSS (2DS). Furthermore, carvedilol pretreatment inhibited ADR-induced increase in plasma troponin I and LDH. CONCLUSIONS: These results suggested a protective role of carvedilol against ADR-induced cardiotoxicity.

The Adverse Reactions of Pfizer BioNTech COVID-19 Vaccine Booster Dose are Mild and Similar to the Second Dose Responses: A Retrospective Cross-Sectional Study.

Background: Like other vaccines, Pfizer BioNTech's COVID-19 vaccine efficacy against SARS-CoV-2 virus infections begins to decline within a few months after the 2nd dose. On August 12, 2021, the FDA allowed additional Pfizer BioNTch's COVID-19 vaccine dose (3rd or booster dose) for individuals with weakened immunity. This study aimed to evaluate the short-term adverse reactions (ADRs) of the 2nd and the 3rd doses of the Pfizer BioNTech COVID-19 vaccine. Methods: Information for this study was collected by Google Form questionnaire (online survey). The results included responses from 442 people, the majority from Saudi Arabia. Results: The most common local ADRs following the 3rd dose were injection site pain, injection site hypersensitivity, and axillary lymph node swelling. The most common systemic ADRs were fatigue, muscle pain, bone pain, headache, and fever less than 38ºC. Less common systemic ADRs were shivering, fever more than 38ºC, nasal congestion and rhinorrhea, arrhythmia, cough, abdominal pain, chest tightness, nausea, diarrhea, vomiting, and tachypnea. Rare systemic ADRs were constipation, dizziness and vertigo, lack of concentration, sore throat, excessive hair loss, dysmenorrhea and heavy menstruation, and Bell's palsy. Severe allergic reactions were reported by 2.6% of participants after the 2nd dose, compared with none after the 3rd dose. Nasal congestion and runny nose are more frequent after the 3rd dose. The ADRs of the 2nd and 3rd doses were significantly more prevalent in females. 12% of participants reported ADRs lasting more than one week after the 3rd dose compared to 5% after the 2nd dose. People ≤ 60 years were more affected by the vaccine ADRs. Conclusion: Most of the ADRs reported after the 3rd vaccine dose were consistent with the Pfizer vaccine information sheet and similar to the 2nd dose ADRs.

Captopril downregulates expression of Bax/cytochrome C/caspase-3 apoptotic pathway, reduces inflammation, and oxidative stress in cisplatin-induced acute hepatic injury.

Cisplatin (Cis) is an effective cancer therapy commonly employed in many therapeutic regimens. However, treatment regimens that contain either a high dose or cumulative doses of Cis could trigger liver damage. A unique study demonstrated that captopril (Cap) protects against Cis-induced liver toxicity, but only some liver function enzymes and some antioxidant enzymes were investigated in that study. Our study aims to elucidate the protective mechanism of Cap against Cis liver toxicity. Acute liver toxicity was induced in rats by injecting a single Cis dose (7.5 mg/kg) in three groups (n = 6). Two groups were pre-treated with low (50 mg/kg) and high (100 mg/kg) Cap doses for one week before Cis injection, and the third group was injected with Cis only. The high Cap dose significantly improved liver function markers (ALT, AST, and ALP) and hepatic tissue pathology. The low Cap dose significantly improved ALP and, to a lesser extent, hepatic tissue pathology. Both Cap doses significantly decreased liver contents of MDA, IL-1ß, and cleaved caspase-3; and liver protein expression of TNF-α, Bax, and caspase-3. The high Cap dose significantly increased liver contents of GSH, GPx, CAT, and SOD, and the liver protein expression of Bcl2. Moreover, only the high Cap dose significantly decreased liver IL-6 content and cytochrome C protein expression. Cap did not inhibit the antitumor impact of Cis against HCT116 cancer cells. Therefore, Cap restricts Cis-induced liver toxicity by reducing inflammation and apoptosis and augmenting the antioxidant system.

Chamomile flower extract ameliorates biochemical and histological kidney dysfunction associated with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is the most prevalent endocrine disorder in females of childbearing age and research findings have revealed a potential association between PCOS and renal dysfunction. This study aimed to investigate renal dysfunction that might be associated with PCOS in rats and to evaluate the potential protective effect of chamomile against PCOS complicated by kidney damage. A rat model of PCOS was induced by injecting estradiol valerate (0.2 mg/rat × 2) into adult virgin female rats. Rats were treated with either ethyl alcohol extract of chamomile flower (75 mg/kg/day) or metformin (Met) (500 mg/kg/day). Induction of PCOS was associated with increased relative right kidney weight percentage and increased serum levels of urea, lipid peroxide product, and testosterone. PCOS was also associated with increased p53 expression in kidney glomeruli and medullary tubules with decreased Bcl2 expression in kidney glomeruli. Administration of chamomile extract significantly decreased levels of serum urea, testosterone, and lipid peroxide product, and p53 expression in kidney glomeruli and tubules. The extract significantly increased levels of antioxidant markers levels (reduced glutathione, catalase, and superoxide dismutase) and the expression of the anti-apoptotic gene Bcl2. Conversely, administration of Met did not improve serum levels of urea. Met also exerted no pronounced effect on p53 gene expression. The results of this study highlight the importance of monitoring kidney function in patients with PCOS and investigating the associated underlying mechanism. Chamomile extract was found to ameliorate kidney damage associated with PCOS through antioxidant, testosterone-lowering, and anti-apoptotic mechanisms.

Vitamin E and 5-amino salicylic acid ameliorates acrylamide-induced peripheral neuropathy by inhibiting caspase-3 and inducible nitric oxide synthase immunoexpression.

Acrylamide is a fundamental cause of accidental toxicity in humans. This study aimed to investigate the neuroprotective effect of vitamin E (Vit. E), 5-amino salicylic acid (5-ASA), and their combination against acrylamide-induced sciatic nerve toxicity. For this purpose, 25 male Wister rats were divided into 5 groups: control, acrylamide, acrylamide + Vit. E, acrylamide + 5-ASA, and acrylamide + Vit. E + 5-ASA. Food intake and body weight were assessed after 7 days. Furthermore, the gait score was also evaluated for each rat. The sciatic nerve was dissected, fixed, and processed for routine light and electron microscopic examination. Haematoxylin and eosin, osmium tetroxide for myelin sheath, and toluidine blue for semithin section were used. In addition, immunohistochemistry for caspase-3 and inducible nitric oxide synthase (iNOS) were performed. The results showed reduced food intake and body weight in acrylamide rats. Abnormal gait score was also recorded in acrylamide rats with significant improvement in Vit. E, and Vit. E + 5-ASA groups. Histologically, Vit. E and 5-ASA provided potential protection against decreased sciatic nerve axon density, disrupted myelination, and the alteration in the immunohistochemistry induced by acrylamide. Vit. E and its combination with 5-ASA provided more evident protection compared to 5-ASA alone. 5-ASA significantly decreased apoptotic cell death (caspase-3 immunoexpression) while Vit. E failed. Both Vit. E and 5-ASA significantly decreased iNOS immunoexpression in the sciatic nerve, where 5-ASA was superior to Vit. E. These findings concluded that both Vit. E and 5-ASA protect against acrylamide-induced peripheral neuropathy through downregulation of both caspase-3 and iNOS immunoexpression.

The Impact of ABO Blood Grouping on COVID-19 Vulnerability and Seriousness: A Retrospective Cross-Sectional Controlled Study among the Arab Community.

Background and Objectives: Studies have noted that some ABO blood types are more susceptible to COVID-19 virus infection. This study aimed to further confirm the relationship between different blood groups on the vulnerability, symptoms, cure period, and severity among COVID-19 recovered patients. Subjects and Methods: This cross-sectional study approached the participants from the Arab community via social media (mainly Facebook and WhatsApp). The data were collected through two Google Form questionnaires, one for COVID-19 recovered patients (COVID-19 group, n = 726), and the other for the healthy people (Control group, n = 707). Results: The subjects with blood group O were the least likely to be infected with the COVID-19 virus, while those with blood group A were not likely to be the most susceptible. There were significant differences among different ABO blood groups regarding the distribution of oxygen saturation percentage, myalgia, and recovery time after COVID-19 infection (p < 0.01, 0.01, and 0.05, respectively). The blood group A showed the highest percentage of patients who experienced an oxygen saturation range of 90-100%, whereas the blood group O showed the highest percentage of patients who experienced an oxygen saturation range of 70-80%. The blood group A showed the lowest percentage of patients who required artificial respiration, whereas the blood group O showed the highest percentage of patients who required artificial respiration. The blood group B showed the lowest percentage of patients who experienced myalgia and exhibited the lowest percentage of patients who needed 3 weeks or more to recover. Conclusion: The people of blood group O may be the least likely to be infected with COVID-19, however, they may be the more in need of treatment in hospital and artificial respiration compared to the other blood groups.