The preventive effects of Ulva lactuca aqueous extract, ulvan polysaccharides and atorvastatin on ethylene glycol-induced hyperoxaluria.

OBJECTIVE: Kidney stones are a common complication of hyperoxaluria. The aim of this study is to investigate the protective and preventive effects of Ulva lactuca aqueous extract, ulvan polysaccharides and atorvastatin on ethylene glycol-induced hyperoxaluria. MATERIALS AND METHODS: Male Wistar rats between 110 and 145 g in weight were used in the study, Ulva lactuca aqueous extract and polysaccharides were prepared. The male albino rats were supplemented with 0.75 percent ethylene glycol (v/v) in their drinking water for six weeks to induce hyperoxaluria. Ulvan infusions (100 mg/kg body weight), ulvan polysaccharides (100 mg/kg body weight), and atorvastatin (two milligrams/kg body weight) to treat hyperoxaluric rats for four weeks (every other day) were used. Weight loss, serum creatinine, serum urea, serum uric acid, serum oxalate, kidney oxalate, kidney lipid peroxidation, and kidney DNA fragmentation and kidney histopathological studies were done. RESULTS: Weight loss, rise of serum creatinine, serum urea, serum uric acid, serum oxalate, kidney oxalate, kidney lipid peroxidation, and kidney DNA fragmentation were all shown to be prevented by the addition of atorvastatin, polysaccharides, or aqueous extract, respectively. Catalase (CAT) activity, glutathione peroxidase (GPX) activity, glutathione-S-transferase (GST) activity, and histopathological perturbations were all significantly reduced by the medicines that were studied. CONCLUSIONS: Hyperoxaluria caused by ethylene glycol may be prevented by a combination of Ulva lactuca aqueous extract, ulvan polysaccharides, and atorvastatin. A reduction in renal oxidative stress and an improvement of the antioxidant defense system may be responsible for these protective benefits. However, Ulva lactuca infusion and ulvan polysaccharides need to be studied further in humans, in order to determine their efficacy and safety.

Platelet-Rich Plasma Ameliorates Monosodium Iodoacetate-Induced Ankle Osteoarthritis in the Rat Model via Suppression of Inflammation and Oxidative Stress.

Until now, there is no treatment that cause complete cure of the chronic inflammatory and degenerative disease, osteoarthritis (OA). Moreover, the underlying mechanisms of OA development and progress are not fully elucidated, and the present pharmacological treatment alternatives are restricted and associated with adverse side effects. Thus, the present study was conducted to evaluate the role of platelet-rich plasma (PRP) in the remedy of OA in the rat model in terms of inflammation, ankle histopathological alterations, and oxidative stress. OA was induced in male Wistar rats by injection of MIA (2 mg)/50 µL isotonic saline in the right ankle joint for two successive days in each rat. After the 2nd MIA injection, the osteoarthritic rats were allocated into two groups such as the MIA group (group 2) and MIA + PRP group (group 3). The MIA + PRP group was treated with PRP (50 µL) by injection into the ankle joint of the right hind limb of each rat at days 14, 21, and 28 after the 2nd injection of MIA. The same equivalent volume of saline, as a substitute of PRP, was injected into the ankle joint of each rat of the normal control group (group 1) and MIA group (group 2) at the same tested periods. Swelling of joint, bodyweight, total leucocytes count (TLC), and morphological as well as histological changes of ankle joints were evaluated. Serum lipid peroxides (LPO), glutathione (GSH), and glutathione S-transferase (GST) levels were examined as biomarkers of oxidative stress. Serum tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), and interleukin-4 (IL-4) were investigated by ELISA as biomarkers of inflammation. In addition, magnetic resonance imaging (MRI) was carried out to investigate the soft tissues in joints. The obtained results revealed that PRP reduced LPO and increased GSH and GST levels in osteoarthritic rats. Also, PRP significantly diminished serum TNF-α and IL-17 levels, while it increased IL-4 serum levels in rats with MIA-induced OA. Morphological observations, histological analysis, and MRI revealed a gradual diminishing in joint inflammation and destruction of cartilage in PRP-injected osteoarthritic rats. Based on these results, it can be suggested that PRP has antiarthritic potential in MIA-induced OA, which may be mediated via suppression of inflammation and oxidative stress.

Thymoquinone and curcumin prevent gentamicin-induced liver injury by attenuating oxidative stress, inflammation and apoptosis.

This study was conducted to assess the preventive effect of two plant constituents, thymoquinone and curcumin, on gentamicin-induced deleterious effect on liver function, integrity and histological architecture. The gentamicin was intraperitoneally injected to rats at dose level of 100 mg/kg b.w. (every other day) for 21 days. The thymoquinone and curcumin were concurrently and orally administered at dose level of 20 mg/kg b.w. (every other day) to gentamicin-injected rats. The present data indicated that thymoquinone and curcumin significantly prevented the gentamicin-induced elevations of serum AST, ALT and LDH activities as well as tumor necrosis factor alpha (TNF-α) and total bilirubin levels. On the other hand, both agents markedly ameliorated the gentamicin-induced decrease in serum total protein, albumin and albumin/globulin ratio. In addition, the gentamicin-induced liver histological alterations including hydropic degeneration of hepatocytes, fatty changes, inflammatory cell infiltration and congestion of portal vein were successfully amended by thymoquinone and curcumin. The elevated proapoptotic proteins caspase 3 and Bax expression in cytoplasm and nucleus of hepatocytes of gentamicin-injected rats were reduced to normal value as a result of thymoquinone and curcumin administration while the lowered expression of antiapoptotic protein Bcl-2 was increased. Based on the previous findings, it can be concluded that thymoquinone and curcumin successfully prevents the deleterious effects on liver function and histological integrity to more or less the same degree by enhancing anti-oxidant defense system, suppression of oxidative stress and attenuation of inflammation and apoptosis.

The toxicity of Capparis tomentosa in sheep and calves.

Five Desert sheep and three Zebu calves were poisoned with daily oral doses of the dry leaves of Capparis tomentosa and died or were killed in extremis at various times after the commencement of dosing. The important clinical signs of Capparis poisoning in sheep and calves were weakness of the hind limbs, staggering, swaying, flexion of the fetlock and phalangeal joints, pain in the sacral region, inappetence and recumbency. There was decrease in the level of total protein and calcium and an increase of glutamic oxaloacetic transaminase (GOT), ammonia, sodium and potassium in serum. The main pathological changes were vacuolation of the neurons and axons in the spinal cord, with necrosis of the centrilobular hepatocytes and renal convoluted tubules and glomeruli.