Knowledge of Sickle Cell Disease Among Medical Students at Al-Baha University, Saudi Arabia: A Cross-Sectional Study.

BACKGROUND: Sickle cell disease (SCD) presents a major health challenge in Saudi Arabia due to its high prevalence. The important role of medical students as future healthcare leaders necessitates high awareness and knowledge about the disease. AIM: To assess SCD awareness among Al-Baha University medical students, and to evaluate its relation to gender and academic level. METHODS: A cross-sectional study was conducted, including 105 medical students from the first to sixth year at Al-Baha University. Data collection utilized an online self-administered questionnaire, covering demographic characteristics and assessing SCD knowledge. Fisher's exact and Pearson Chi-squared tests were employed to analyze associations between gender, academic level, and SCD awareness. RESULTS: The majority of male participants 52 (89.6%) and all females 47 (100%) demonstrated awareness of SCD. Clinical year enrollment (68.6%) correlated with heightened awareness across various aspects of SCD compared to the preclinical year. Most participants were in clinical years (68.6%), and 94.3% of them had knowledge about SCD. Approximately, 75 (71%) of participants correctly identified features of sickle cell crisis, 83 (79%) reported the accurate cause of SCD, and 75 (71%) cited the appropriate preventive measures. Only 15 (14%) demonstrated knowledge of correct management of SCD. Contrarily, 84 (80%) were aware of SCD complications, 66 (63%) recognized different SCD types, 67 (64%) felt adequately informed about SCD, and 34 (32%) were involved in SCD counseling. Male participants exhibited greater awareness of SCD features than females. Notably, involvement in SCD counseling was more prevalent among students of clinical years. CONCLUSION: This study underscores the need for targeted educational initiatives, particularly among preclinical year students to enhance SCD awareness among students. We also emphasize the role of clinical education in fostering a comprehensive understanding of SCD, with increased participation in counseling programs.

Intramedullary Kirschner wire fixation of displaced distal forearm fractures in children.

AIM OF THE WORK: This study was designed to highlight internal fixation by intramedullary K-wires for displaced distal forearm fractures among children and analyze the results of this technique. We hypothesize that physis-sparing intramedullary fixation prevents displacement with a lower complication rate. METHODS: This prospective case series involving 47 patients was conducted between February 2018 and December 2019. All patients with open physis presented with recent displaced distal forearm fractures were included, and all of them were treated with an intramedullary k-wire fixation for both bones with the assessment of the union rate, union time, suspected complication, radiographic evaluation, and functional outcome. RESULTS: The study population consisted of 31 boys (66%) and 16 girls (34%). The mean age of the patients was 10.68 ± 2.728 years (range, 7-15 years). All fractures were united in a median of 6 weeks (range, 4-8 weeks), The functional outcome after 12 months was normal in 42 patients (89.4%), whereas, in five patients (10.6%), the functional parameters were minimally reduced. The median preoperative angulation improved from 36° (range, 24°-52°) preoperatively to 4° (range, 0°-10°) on immediate postoperative radiographs. After 12 months, the median angulation was 2° (range, 0°-7°) (p < 0.001). The angulation of the distal radius immediately after surgery and at the final follow-up was statistically correlated with the functional outcome (p < 0.001 and 0.002, respectively). CONCLUSION: This technique provides a good result with less susceptibility to re-displacement and low complication rates. LEVEL OF EVIDENCE: Level IV.

Self-Medication Practices Among the General Population in Al-Baha City, Saudi Arabia: A Cross-Sectional Study.

Background The practice of self-medication (SM) is the use of self-consuming medication without consulting healthcare which carries its own risks. SM patterns differ across populations and are influenced by several factors. This study aimed to assess the prevalence of SM practices in Al-Baha, Saudi Arabia, to identify the factors contributing to this practice and develop effective strategies to decrease its occurrence and associated risks. Methodology This cross-sectional study was conducted in Al Baha Province, Saudi Arabia, over two weeks in July 2023, with a sample of 580 participants. Eligible participants were males and females, both Saudi and non-Saudi, aged 18-65. The data were collected using a self-administered online questionnaire. Results Of all participants, 48.7% admitted taking medications without a healthcare practitioner's prescription in the last three months. Analgesics were the most common SM (29.1%), followed by vitamins and minerals (16.2%), and antipyretics (14.1%). The side effects experienced from SM included nausea (24.5%), headache (20.5%), and shortness of breath (8.7%). Regarding the source of medication, the majority (61.9%) obtained medications from a pharmacy and 14.6% used existing stock. Age was significantly associated with higher rates in the 18-29 and 40-49 age groups. Educational status was significantly associated with higher SM among graduates. Regarding reading medical instructions, 39.2% always read, 47.7% sometimes read, and 13.1% never read. Regarding antibiotic SM, 61 participants reported using over-the-counter (OTC) antibiotics. Common reasons for use included sore throat (27.8%) and common cold (19.6%). The most common reason for SM was to save time (25.9%), followed by avoiding crowds and long waits (17.1%). Conclusions A significant prevalence of SM practice concerning antibiotic misuse and sex differences with female dominance was detected. We recommend further public awareness activities from related organizations and more regulations for OTC prescription practices to ensure safe SM practices. In addition, further research is needed to explore SM patterns.

Minimally Invasive Reconstruction of the Medial Collateral Ligament of the Knee.

Background: This study describes a minimally invasive technique for the reconstruction of the medial collateral ligament (MCL) and posterior oblique ligament (POL) through minimal incisions on the tibial and femoral sides of the ligament using the modified Bosworth technique. Methods: This study included 19 consecutive patients who presented with chronic grade III injury; the mean age was 29.6 years (standard deviation ± 7.5 years, range 19-43 years), and five patients (26.3%) had no associated injuries. Ten patients (52.6%) had associated anterior cruciate ligament (ACL) injury and four patients (21.1%) had associated posterior cruciate ligament (PCL) injury. All patients were assessed 18 months postoperatively regarding functional outcome using the Lysholm score and medial joint space opening. Results: There was a statistically significant improvement in the patient functional outcome as the Lysholm score improved from 55.39 ± 6.9 to 89.42 ± 6.4 at 18 months postoperatively. (P< 0.001). At the end of the follow-up, 16 cases had grade 1 medial laxity, 3 cases with grade II laxity, and no patients with grade III medial laxity. Conclusion: Minimally invasive MCL reconstruction with modified Bosworth technique gives very good results regarding the functional outcome and residual medial laxity of the knee.

Hesperidin opposes the negative impact of cyclophosphamide on mice kidneys.

The present investigation examined the prospective nephroprotective effect of hesperidin (HSN) in mice challenged with a single i.p. injection of cyclophosphamide (CPE) at a dose of 200 mg/kg. HSN (100 and 200 mg/kg/day, p.o.) was given for 10 days, starting 5 days prior to CPE administration. HSN significantly reduced the CPE-induced increments of serum creatinine and cystatin C. HSN also significantly reduced malondialdehyde, nitric oxide, Bax/Bcl-2 ratio, and caspase-3, and significantly raised total antioxidant capacity, and interleukin-10/tumor necrosis factor-α ratio in kidneys of mice received CPE. In addition, HSN significantly prevented the histopathological injury, and kidney injury molecule-1 expression in kidneys of mice given CPE. It was concluded that HSN guarded against nephrotoxic effect of CPE in mice by tackling oxidative/nitrative stress, inflammation, and apoptosis.

Diacerein Downregulates NLRP3/Caspase-1/IL-1ß and IL-6/STAT3 Pathways of Inflammation and Apoptosis in a Rat Model of Cadmium Testicular Toxicity.

The potential gonadal protective effect of diacerein (DCN) and its underlying mechanisms were studied in a rat model of cadmium-induced testicular toxicity. The rats received DCN (50 mg/kg/day, p.o.) for 10 days and one injection of CdCl2 (2 mg/kg, i.p.) on day 9. Cadmium significantly declined serum testosterone and significantly raised interleukin-1ß, interleukin-6, interleukin-18, tumor necrosis factor-α, caspase-1, phosphorylated signal transducer and activator of transcription-3 (pSTAT3), nuclear factor-κB p65, Bax, and caspase-3 in rat testes. DCN significantly ameliorated the changes in the biochemical measurements observed with CdCl2 insult. Additionally, DCN preserved the normal testicular architecture, maintained spermatogenesis, and lowered the expression of NOD-like receptor family protein 3 (NLRP3) inflammasome in testes of rats that received CdCl2. It was concluded that DCN significantly protected the gonads of male rats exposed to cadmium toxicity through modulation of NLRP3/caspase-1/IL-1ß and IL-6/STAT3 pathways of inflammation and apoptosis.

Naringenin palliates cisplatin and doxorubicin gonadal toxicity in male rats.

Cisplatin (CP) and doxorubicin (DX) can cause testicular injury by inducing oxidative/nitrosative stress, inflammation, and apoptosis, Naringenin (NG) has antioxidant, antinitrative, anti-inflammatory, and anti-apoptotic effects. This study investigated the potential ability of NG to block gonadotoxicity induced CP and DX in male rats. The rats received one injection of either CP (10 mg/kg, i.p.) or DX (15 mg/kg, i.p.), and treated with NG (50 mg/kg/day, p.o.) for 10 days beginning 6 days prior to CP and DX administration. NG significantly prevented the decreases of serum testosterone and inhibin B in rats received CP and DX. Additionally, NG significantly decreased the elevated testicular malondialdehyde, tumor necrosis factor-α/interleukin-10 ratio, and caspase-3 in CP- and DX-treated rats. NG also significantly raised the decreased testicular Bcl-2/Bax ratio, and total antioxidant status in CP- and DX-challenged rats. In addition, NG significantly increased P-glycoprotein level in testes of rats received CP and DX. Moreover, NG significantly decreased the testicular histopathological injury, and immunohistochemical expression of inducible nitric oxide synthase induced by CP and DX in rat testes. It was concluded that NG impeded gonadotoxicity of CP and DX in male rats by mitigating oxidative stress, nitrosative stress, inflammation, and apoptosis.

Therapeutic effect of carnosine in rat model of experimental liver carcinogenesis.

The possible anticancer effect of carnosine versus doxorubicin was investigated against hepatocellular carcinoma (HCC) induced by trichloroacetic acid (TCA) (500mg/kg/day, p.o., for 5days) in rats. Following induction of HCC, rats treated with either carnosine (10mg/kg/day, i.p.), or doxorubicin (2.5mg/kg, i.p., once weekly), for 2 weeks. Carnosine significantly decreased serum alanine aminotransferase, and hepatic lipid peroxidation, nitric oxide, tumor necrosis factor-α, and nuclear factor-κB p65 unit, and significantly increased liver total antioxidant status in TCA-challenged rats. The effects of doxorubicin on oxidative, nitrative, and inflammatory biomarkers were less significant than carnosine. However, both carnosine and doxorubicin significantly induced liver tissue apoptotic biomarkers, Bax, cytosolic cytochrome C, and caspase-3, in a comparable manner. Additionally, carnosine and doxorubicin reduced the histopathological dysplastic changes, and alpha-fetoprotein expression in liver of rats with HCC. It was concluded that carnosine significantly protected against TCA-induced liver carcinogenesis in rats, through its antioxidant, antinitrative, and anti-inflammatory effects, and induction of apoptosis.

Epigallocatechin-3-gallate counters cisplatin toxicity of rat testes.

CONTEXT: Epigallocatechin-3-gallate (EG), the main active flavonoid in green tea, has well-known anti-inflammatory, antioxidant, and anti-apoptotic activities. OBJECTIVE: The EG protection against testicular injury induced by cisplatin was studied in Sprague-Dawley rats. MATERIALS AND METHODS: Cisplatin (10 mg/kg, i.p) was given as a single injection to rats. EG was given at 40 and 80 mg/kg/day, i.p., for 5 days, starting the same day of cisplatin insult. Serum testosterone, and testicular malondialdehyde, total antioxidant status, nitric oxide, interleukin-6, interleukin-1ß, cytochrome C, Bax/Bcl-2 ratio, and caspase-3 were measured. In addition, testicular histopathological examination and immunohistochemical expression of testicular tumour necrosis factor-α were evaluated. RESULTS: Cisplatin, compared to the control, significantly decreased serum testosterone (6.48 ± 0.7 vs. 50.8 ± 4.91 ng/10 mL), and testicular tissue antioxidant status (17.3 ± 1.21 vs. 64.12 ± 5.4 µmol/g), and significantly increased interleukin-6 (85.81 ± 6.11 vs. 38.2 ± 2.79 pg/100 mg), interleukin-1ß (98.09 ± 8.31 vs. 32.52 ± 2.08 pg/100 mg), malondialdehyde (74.5 ± 5.88 vs. 23.8 ± 1.91 nmol/g), nitric oxide (104.98 ± 8.5 vs. 52.68 ± 5.12 nmol/100 mg), cytochrome C (5.97 ± 0.33 vs. 1.6 ± 0.99 ng/mg protein), Bax/Bcl-2 ratio (4.01 ± 0.38 vs. 0.71 ± 0.0), and caspase-3 (3.2 ± 0.21 vs. 0.98 ± 0.08 O.D. 405 nm) in rat testes. EG (40 and 80 mg/kg, respectively) caused significant increases of serum testosterone (33.9 ± 2.89 and 47.88 ± 4.4 ng/10 mL), and testicular antioxidant status (47.1 ± 3.92 and 58.22 ± 3.58 µmol/g), and significant decreases of interleukin-6 (57.39 ± 4.2 and 48.18 ± 3.98 pg/100 mg), interleukin-1ß (65.12 ± 5.88 and 41.96 ± 3.51 pg/100 mg), malondialdehyde (42.3 ± 3.9 and 28.67 ± 2.49 nmol/g), nitric oxide (70.6 ± 6.79 and 61.31 ± 5.18 nmol/100 mg), cytochrome C (3.4 ± 0.27 and 2.21 ± 0.18 ng/mg protein), Bax/Bcl-2 ratio (1.49 ± 0.14 and 1.1 ± 0.09), and caspase-3 (2.1 ± 0.17 and 1.48 ± 0.13 O.D. 405 nm) in testes of cisplatin-treated rats. Additionally, both doses of EG significantly ameliorated the histopathological injury and reduced tumour necrosis factor-α expression in rat testes. CONCLUSION: EG can afford testicular protection in cisplatin-challenged rats by its antioxidant, antinitrative, anti-inflammatory and antiapoptotic effects.

Nephroprotection of punicalagin in rat model of endotoxemic acute kidney injury.

The potential nephroprotection of punicalagin (PNG) against lipopolysaccharide (LPS)-induced acute kidney injury in rats was investigated. Rats received a single i.v. dose of LPS (5 mg/kg), and treated with PNG (50 mg/kg, i.p.), 1 h before, and 1 h following LPS administration. LPS caused significant increases of serum creatinine and neutrophil gelatinase-associated lipocalin. LPS also resulted in significant increases in interleukin-18, tumor necrosis factor-α, interleukin-6, malondialdehyde, nitric oxide, Bax/Bcl-2 ratio and myeloperoxidase, inducible nitric oxide synthase, caspases 3, 8 and 9 activities, and a significant decrease in total antioxidant capacity in kidney tissues. PNG significantly ameliorated the alterations in the measured parameters. Additionally, PNG attenuated the histopathological injury and reduced kidney injury molecule-1 expression in kidneys of rats that received LPS. It was concluded that PNG ameliorated endotoxemic acute kidney injury in rats by counteracting inflammation, oxidative/nitrative stress and apoptosis.

Punicalagin alleviates hepatotoxicity in rats challenged with cyclophosphamide.

This study investigated the possible hepatoprotection of punicalagin in rats received cyclophosphamide (20mg/kg/day, i.p., for 7 days). Punicalagin given at two doses, 15 and 30mg/kg/day, p.o., for 7 days, starting the same day of cyclophosphamide administration. Punicalagin significantly and dose-dependently reduced the elevations of serum alanine aminotransferase, and liver nuclear factor-κB p65, tumor necrosis factor-α, interleukin-1ß, malondialdehyde, nitric oxide, Bax/Bcl-2 ratio, inducible nitric oxide synthase, caspases 3 and 9 activities, and prevented the decrease of hepatic total antioxidant capacity. Punicalagin also attenuated the histopathological liver tissue damage, and decreased cyclooxygenase-2 expression in liver of rats received cyclophosphamide in a dose-dependent manner. It was concluded that punicalagin protected rat liver against cyclophosphamide toxicity by inhibiting oxidative/nitrosative stress, inflammation, and apoptosis.

Protective Effect of Naringenin against Lipopolysaccharide-Induced Acute Lung Injury in Rats.

BACKGROUND/AIMS: Lipopolysaccharide (LPS) induces acute lung injury (ALI) through oxidative stress and inflammation. Naringenin exerts antioxidant and anti-inflammatory effects. The possible protective effect of naringenin was investigated against ALI induced by LPS in rats. METHODS: Rats received a single injection of LPS (5 mg/kg, i.v.). Naringenin was given for 4 consecutive days, at 2 doses (50 and 100 mg/kg/day, p.o.), starting 3 days before LPS administration. RESULTS: LPS significantly increased wet/dry lung weight ratio, malondialdehyde, nitric oxide (NO), interleukin-6, and myeloperoxidase activity in the lung tissues. Naringenin, particularly the higher dose, significantly ameliorated the LPS-induced changes in the measured parameters. Also, naringenin markedly reduced the histopathological lung tissue injury that resulted from LPS. Naringenin significantly decreased the LPS-induced expression of nuclear factor-x03BA;B, inducible NO synthase, tumor necrosis factor-α, caspase-3, and significantly increased heat shock protein 70 expression in the lungs. CONCLUSION: Naringenin significantly protected against LPS-induced ALI in rats through its anti-inflammatory, antioxidant, antinitrosative, and antiapoptotic effects.

Ameliorative effects of thymoquinone against eye lens changes in streptozotocin diabetic rats.

The possible protective effect of thymoquinone against eye lens changes in diabetic rats was investigated. Following diabetes induction by a single injection of streptozotocin (45 mg/kg, i.p.), thymoquinone was administered in three different doses (20, 40, and 80 mg/kg/day, p.o.) for 12 weeks. Thymoquinone significantly and dose-dependently attenuated the hypoinsulinemia and hyperglycemia in diabetic rats. Also, thymoquinone (particularly 40 and 80 mg/kg) significantly decreased the elevations of malondialdehyde, nitric oxide, tumor necrosis factor-α, glycated proteins, aldose reductase activity, sorbitol level, and caspase-3 activity in the lens tissues of diabetic rats. In addition, thymoquinone (particularly 40 and 80 mg/kg) significantly ameliorated the diabetes-induced reductions of glutathione peroxidase, superoxide dismutase, and catalase activities, and total and soluble protein contents in the lens tissues. It was concluded that thymoquinone significantly protected the lens tissue against changes induced by diabetes in rats through its antioxidant, anti-inflammatory, and antidiabetic effects.

Protective effect of telmisartan treatment against arsenic-induced testicular toxicity in rats.

Oxidative/nitrosative stress, inflammation, and apoptosis play a crucial role in the pathogenesis of arsenic-induced testicular injury. Telmisartan, the angiotensin II-receptor antagonist, possesses antioxidant and anti-inflammatory activities. The protective effect of telmisartan against arsenic-induced testicular damage was investigated in rats. Testicular damage was induced by sodium arsenite (10 mg kg-1/day, p.o., for 2 consecutive days). Telmisartan (10 mg kg-1/day, i.p.) was given for 3 consecutive days, starting 1 day before sodium arsenite administration. Telmisartan significantly attenuated the arsenic-induced decrease in the levels of serum testosterone and testicular reduced glutathione, and significantly decreased the elevation of the levels of testicular malondialdehyde, nitric oxide, and arsenic levels, as well as myeloperoxidase activity resulting from sodium arsenite administration. Histopathological and immunohistochemical examination revealed that telmisartan markedly attenuated testicular tissue changes, and decreased the arsenic-induced expression of vascular endothelial growth factor, inducible nitric oxide synthase, tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB, and caspase-3. Telmisartan, via its antioxidant and/or anti-inflammatory effects, may represent a potential candidate to protect against the deleterious effects of arsenic on testicular tissue.

Protective effect of naringenin against gentamicin-induced nephrotoxicity in rats.

The protective effect of naringenin, a flavonoid compound isolated from citrus fruits, was investigated against nephrotoxicity induced by gentamicin (80mgkg(-1)/day, i.p., for eight days) in rats. Naringenin treatment (50mgkg(-1)/day, p.o.) was administered for eight days, starting on the same day of gentamicin administration. Gentamicin caused significant elevations of serum creatinine, and kidney tissue levels of malondialdehyde, nitric oxide, and interleukin-8, and a significant decrease in renal glutathione peroxidase activity. Naringenin treatment significantly ameliorated the changes in the measured biochemical parameters resulted from gentamicin administration. Also, naringenin markedly attenuated the histopathological renal tissue injury observed with gentamicin. Immunohistochemical examinations showed that naringenin significantly reduced the gentamicin-induced expression of kidney injury molecule-1, vascular endothelial growth factor, inducible nitric oxide synthase, and caspase-9, and increased survivin expression in the kidney tissue. It was concluded that naringenin, through its antioxidant and anti-inflammatory effects, may represent a therapeutic option to protect against gentamicin nephrotoxicity.

Protective effect of cannabidiol against cadmium hepatotoxicity in rats.

The protective effect of cannabidiol, the non-psychoactive component of Cannabis sativa, against liver toxicity induced by a single dose of cadmium chloride (6.5 mgkg(-1) i.p.) was investigated in rats. Cannabidiol treatment (5 mgkg(-1)/day, i.p.) was applied for five days starting three days before cadmium administration. Cannabidiol significantly reduced serum alanine aminotransferase, and suppressed hepatic lipid peroxidation, prevented the depletion of reduced glutathione and nitric oxide, and catalase activity, and attenuated the elevation of cadmium level in the liver tissue resulted from cadmium administration. Histopathological examination showed that cadmium-induced liver tissue injury was ameliorated by cannabidiol treatment. Immunohistochemical analysis revealed that cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue. It was concluded that cannabidiol may represent a potential option to protect the liver tissue from the detrimental effects of cadmium toxicity.

Cardioprotective effect of cannabidiol in rats exposed to doxorubicin toxicity.

The potential protective effect of cannabidiol, the major non-psychotropic Cannabis constituent, was investigated against doxorubicin cardiotoxicity in rats. Cardiotoxicity was induced by six equal doses of doxorubicin (2.5mgkg(-1) i.p., each) given at 48h intervals over two weeks to achieve a total dose of 15mgkg(-1). Cannabidiol treatment (5mgkg(-1)/day, i.p.) was started on the same day of doxorubicin administration and continued for four weeks. Cannabidiol significantly reduced the elevations of serum creatine kinase-MB and troponin T, and cardiac malondialdehyde, tumor necrosis factor-α, nitric oxide and calcium ion levels, and attenuated the decreases in cardiac reduced glutathione, selenium and zinc ions. Histopathological examination showed that cannabidiol ameliorated doxorubicin-induced cardiac injury. Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, nuclear factor-κB, Fas ligand and caspase-3, and increased the expression of survivin in cardiac tissue of doxorubicin-treated rats. These results indicate that cannabidiol represents a potential protective agent against doxorubicin cardiac injury.

Simvastatin treatment ameliorates injury of rat testes induced by cadmium toxicity.

Cadmium-induced testicular toxicity is mediated through oxidative stress and inflammation which eventually lead to cell death. Simvastatin, the antihyperlipidemic agent, exhibits additional antioxidant and anti-inflammatory activities. The aim of the present work was to investigate the protective effect of simvastatin against cadmium-induced testicular toxicity in rats. The rats received a single intraperitoneal (i.p.) injection of cadmium chloride (2 mg/kg). Simvastatin treatment (5 mg/kg/day, i.p.) was applied for three consecutive days, starting 1 day before cadmium administration. Cadmium significantly decreased serum testosterone, and testicular reduced glutathione and catalase activity, and significantly increased testicular malondialdehyde, nitric oxide, and cadmium ion levels. Simvastatin significantly ameliorated the biochemical changes induced by cadmium. Cadmium-induced testicular tissue injury observed by histopathological examination was attenuated by simvastatin. In addition, simvastatin significantly decreased the expression of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, nuclear factor-κB, and caspase-3, and increased heme oxygenase-1 expression in testicular tissue of rats exposed to cadmium toxicity. It was concluded that simvastatin, through its antioxidant and anti-inflammatory activities, provided a significant protective effect against cadmium-induced testicular toxicity in rats. However, starting treatment with simvastatin before cadmium exposure, as done in the present work, is not clinically applicable. Therefore, other investigations are needed to assess the protective effect of simvastatin treatment following induction of cadmium testicular toxicity.

Therapeutic effect of coenzyme Q10 against experimentally-induced hepatocellular carcinoma in rats.

The therapeutic potential of coenzyme Q10 was investigated in rats with hepatocellular carcinoma induced by trichloroacetic acid (0.5g/kg/day, p.o., for five days). Coenzyme Q10 treatment (0.4mg/kg/day, i.p.) was applied for four weeks following trichloroacetic acid administration. Coenzyme Q10 significantly suppressed lipid peroxidation, prevented the depletion of reduced glutathione and superoxide dismutase activity, and decreased the elevations of tumor necrosis factor-α and nitric oxide in liver tissue of rats with hepatocellular carcinoma. Also, the histopathological dysplastic changes induced by trichloroacetic acid in liver tissue were ameliorated by coenzyme Q10. Immunohistochemical analysis revealed that coenzyme Q10 significantly decreased the expression of hepPar-1, alpha-fetoprotein, inducible nitric oxide synthase, cyclooxygenase-2 and nuclear factor-κB in liver tissue of rats with hepatocellular carcinoma. It was concluded that coenzyme Q10 may represent a potential therapeutic option for liver carcinogenesis.

Protective effects of captopril in diabetic rats exposed to ischemia/reperfusion renal injury.

OBJECTIVES: To investigate the potential protective effects of captopril, the angiotensin-converting enzyme inhibitor, in diabetic rats exposed to ischaemia/reperfusion (I/R) renal injury. METHODS: Following successful induction of diabetes, captopril treatment (50 mg/kg/day, p.o.) was applied for 4 weeks, after which bilateral renal ischaemia was induced for 30 min followed by reperfusion for 24 h. RESULTS: Captopril significantly attenuated hyperglycaemia and hypoinsulinaemia in diabetic rats, and significantly reduced the elevations of serum creatinine and aldosterone levels, and renal malondialdehyde, tumour necrosis factor-α and nitric oxide (NO), and prevented the depletion of reduced glutathione caused by I/R in diabetic rats. Histopathological renal tissue damage induced by I/R in diabetic rats was ameliorated by captopril treatment. Immunohistochemical analysis revealed that captopril significantly attenuated the reduction of insulin content in pancreatic islet ß-cells, and decreased the I/R-induced expression of inducible NO synthase, nuclear factor-κB, Fas ligand and caspase-3, and increased the expression of survivin and heme oxygenase-1 in the kidney tissue of diabetic rats. CONCLUSIONS: Captopril represents a potential candidate to reduce the risk of renal injury induced by ischaemia/reperfusion in type 2 diabetes.