Characterization of blue green algae isolated from Egyptian rice field with potential anti-hepatitis C active components

Several species of cyanobacteria has been recognized for its therapeutic value that can be used for treatment of malnutrition, cancer and viral infection. Many natural occurring cyanobacteria are known to produce toxins, for example, species of the genera Microcystis, Nodularia, Nostoc, Anabaena, Aphanizomenon, Cylindrospermopsis, and Planktothrix (Oscillatoria). Cyanotoxins are classified according to their mode of action in vertebrates as hepatotoxins, neurotoxins, cytotoxins, dermatotoxins, and irritants. Microcystin is a hepatotoxin which commonly found in Microcystis and it was found to be produced by other genera, including Anabaena, Nostoc, Nodularia, and Planktothrix. In the present study cyanobacteria strain isolated from Egyptian soil was purified, characterized and identified as Nostoc sp. and named Nostoc EGY. PCR-based techniques targeting the toxin biosynthesis genes were used verifying absence of toxic genes in the newly purified cyanobacteria. Cell lysate was prepared from the purified strain; the efficacy of this lysate to prevent hepatitis C virus (HCV) replication in vitro was proved qualitatively and quantitatively. Lysate prepared from isolated cyanobacteria after 10 and 25 days of cultivation was able to prevent replication of in vitro cultivated HCV.Keywords: Hepatitis C, green algae, cyanobacteria, polymerase chain reactionAfrican Journal of Biotechnology, Vol. 13(9), pp. 1086-1096, 26 February, 201

Berberine Reduces Neurotoxicity Related to Nonalcoholic Steatohepatitis in Rats

Berberine is a plant alkaloid that has several pharmacological effects such as antioxidant, antilipidemic, and anti-inflammatory effects. Nonalcoholic steatohepatitis (NASH) triggers different aspects of disorders such as impaired endogenous lipid metabolism, hypercholesterolemia, oxidative stress, and neurotoxicity. In this study, we examined the mechanism by which NASH induces neurotoxicity and the protective effect of berberine against both NASH and its associated neurotoxicity. NASH induced rats showed significant impairments in lipid metabolism with increased serum triglycerides, cholesterol, and low-density lipoprotein (LDL). The NASH induced group also demonstrated a significant oxidative stress which is characterized by increased TBARs level and decreased antioxidant capacity such as GSH and SOD levels. Moreover, the NASH induction was associated with inflammation which was demonstrated by increased TNFα and nitric oxide levels. Hyperglycemia and hyperinsulinemia were observed in the NASH induced group. Also, our results showed a significant increase in the expression of the acetylcholine esterase (AChE) and amyloid beta precursor protein (AβPP). These changes were significantly correlated with decreased insulin degrading enzyme (IDE) and beta-amyloid40 (Aβ40) and increased beta-amyloid42 (Aβ42) in the hippocampal region. Daily administration of berberine (50 mg/kg) for three weeks ameliorated oxidative stress, inflammation, hyperlipidemia, hyperglycemia, hyperinsulinemia, and the observed neurotoxicity

Serum concentration effects on the kinetics and metabolism of hela-s3 cell growth and cell adaptability for successful proliferation in serum free medium

The effect of serum content of culture medium on the kinetics of cell growth and metabolism has been studied in HeLa S3 culture. Increasing the serum concentration from 5 to 15% in Ham’s F12 medium increased the total number of living cells by about 30%. Further increase in serum concentration resulted in significant reduction in viable cell number. Meanwhile, increasing serum concentration in culture medium from 5 to 20% shows positive effect on cell viability and increased it from 38 to 74% in 144 h cultivated cultures. On the other hand, both of glucose consumption and lactate production rates were increased by the increase of serum concentration in the range between 5 and 20%. Based on these data, cells grown in Ham’s F12 medium of 10% serum were used for adaptation to serum free medium (SFM). Successive adaptation of cells to complete SFM was done by cultivating cells in different passages with the increased fraction of SFM in the cultivation medium. The ratios between SM (Ham’s F12 supplemented with 10%) to SFM (SMIF-6) were (100:0; 75:25; 50:50; 25:75; 10:90; 0:100). For each medium, cells were cultivated in 2-3 short passages for only 72 h to keep the cells in all cultures in their mid-exponential phase. Based on this cultivation strategy, HeLa S3 cells were completely adapted to serum free medium in only 880 hours. Neither growth kinetics nor physiological characterization (based on the data of glucose consumption rate and lactate production rate) were changed during the cell adaptation to SFM

PI3K/Akt-independent NOS/HO activation accounts for the facilitatory effect of nicotine on acetylcholine renal vasodilations: modulation by ovarian hormones.

We investigated the effect of chronic nicotine on cholinergically-mediated renal vasodilations in female rats and its modulation by the nitric oxide synthase (NOS)/heme oxygenase (HO) pathways. Dose-vasodilatory response curves of acetylcholine (0.01-2.43 nmol) were established in isolated phenylephrine-preconstricted perfused kidneys obtained from rats treated with or without nicotine (0.5-4.0 mg/kg/day, 2 weeks). Acetylcholine vasodilations were potentiated by low nicotine doses (0.5 and 1 mg/kg/day) in contrast to no effect for higher doses (2 and 4 mg/kg/day). The facilitatory effect of nicotine was acetylcholine specific because it was not observed with other vasodilators such as 5'-N-ethylcarboxamidoadenosine (NECA, adenosine receptor agonist) or papaverine. Increases in NOS and HO-1 activities appear to mediate the nicotine-evoked enhancement of acetylcholine vasodilation because the latter was compromised after pharmacologic inhibition of NOS (L-NAME) or HO-1 (zinc protoporphyrin, ZnPP). The renal protein expression of phosphorylated Akt was not affected by nicotine. We also show that the presence of the two ovarian hormones is necessary for the nicotine augmentation of acetylcholine vasodilations to manifest because nicotine facilitation was lost in kidneys of ovariectomized (OVX) and restored after combined, but not individual, supplementation with medroxyprogesterone acetate (MPA) and estrogen (E2). Together, the data suggests that chronic nicotine potentiates acetylcholine renal vasodilation in female rats via, at least partly, Akt-independent HO-1 upregulation. The facilitatory effect of nicotine is dose dependent and requires the presence of the two ovarian hormones

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats.

BackgroundNeuroinflammation causes neurodegenerative conditions like Alzheimer's disease (AD). Ipriflavone (IP), therapeutic compound to postmenopausal osteoporosis, has limited estrogenic activity and is accounted as AChE inhibitor. The developing of drug delivery systems to enable drug targeting to specific sites increases the drug therapeutic effect.ObjectiveThe aim of the present study was to formulate and evaluate ipriflavone loaded albumin nanoparticles (IP-Np) along with free ipriflavone against lipopolysaccharide (LPS) induced neuroinflammation in rats.MethodsNeuroinflammation was induced by intra-peritoneal (i.p) injection of LPS (250 μg/kg rat body weight) then treatments were conducted with (1) ipriflavone at two doses 50 mg/kg and 5 mg/kg, (2) IP-Np (5 mg ipriflavone/kg) or (3) IP-Np coated with polysorbate 80 (IP-Np-T80) (5 mg ipriflavone/kg). The alteration of the inflammatory response in male adult Wistar rats' brain hippocampus was investigated by examining associated indices using biochemical and molecular analyses.ResultsA significant upsurge in inflammatory mediators and decline in antioxidant status were observed in LPS-induced rats. In one hand, ipriflavone (50 mg/kg), IP-Np and IP-Np-T80 ameliorated LPS induced brain hippocampal inflammation where they depreciated the level of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and enhanced antioxidant status. In another hand, ipriflavone at dose (5 mg/kg) didn't show the same therapeutic effect.ConclusionThe current study provides evidence for the potential neuroprotective effect of ipriflavone (50 mg/kg) against LPS-induced neuroinflammation in rats through its anti-inflammatory and antioxidant activities. Moreover, nanoparticles significantly attenuated neuroinflammation in concentration lower than the effective therapeutic dose of free drug ten times

Cumulative vasodilatory effects of acetylcholine (0.01–2.43 nmol) in phenylephrine (10 µM)-preconstricted isolated perfused kidneys obtained from sham, ovariectomized (OVX) rats supplemented with estrogen (OVX/E2), medroxyprogesterone acetate (OVX/MPA), their combination (OVX/E2/MPA), or the vehicle.

<p>Acetylcholine responses are expressed as percentages of the phenylephrine-induced tone. Values are means±S.E.M. of 6–8 observations. ^*P<0.05 vs. OVX values.</p

Effect of nicotine (0.5–4 mg/kg/day, 2 weeks) on cumulative vasodilatory effects of acetylcholine (0.01–2.43 nmol), NECA (1.6–50 nmol), and papaverine (1–2.43 nmol) in phenylephrine (10 µM)-preconstricted isolated perfused kidneys obtained from sham rats.

<p>Vasodilator responses are expressed as percentages of the phenylephrine-induced tone. Values are means±S.E.M. of 6–8 observations. ^*P<0.05 vs. saline values.</p