The protective effects of curcumin against cigarette smoke-induced toxicity: A comprehensive review.

Cigarette smoking (CS) is a crucial modifiable risk of developing several human diseases and cancers. It causes lung, bladder, breast, and esophageal cancers, respiratory disorders, as well as cardiovascular and metabolic diseases. Because of these adverse health effects, continual efforts to decrease the prevalence and toxicity of CS are imperative. Until the past decades, the impacts of natural compounds have been under investigation on the harmful effects of CS. Turmeric (Curcuma longa), a rhizomatous herbaceous perennial plant that belongs to the Zingiberaceae family, is the main source of curcumin. This review is an attempt to find out the current knowledge on CS's harmful effects and protective potential of curcumin in the pulmonary, liver, brain, gastrointestinal, and testis organs. According to the present review, simultaneous consumption of curcumin and CS can attenuate CS toxicities including chronic obstructive pulmonary disease, gastrointestinal toxicity, metabolic diseases, testis injury, and neurotoxicity. Moreover, curcumin suppresses carcinogenesis in the skin, liver, lungs, breast, colon, and stomach. Curcumin mediates these protective effects through antioxidant, anti-inflammatory, anti-apoptotic, and anti-carcinogenicity properties.

Intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevents the H-89-induced spatial learning deficits in Morris water maze.

OBJECTIVES: H-89 (a protein kinase AII [PKA II] inhibitor) impairs the spatial memory in the Morris water maze task in rats. In the present study, we aimed to study the protective effects of nicotine and O-acetyl-L-carnitine against H-89-induced spatial memory deficits. METHODS: Spatial memory impairment was induced by the bilateral intrahippocampal administration of 10 µM H-89 (dissolved in dimethyl sulfoxide, DMSO) to rats. The rats then received bilateral administrations of either nicotine (1 µg/µL, dissolved in saline) or O-acetyl-L-carnitine (100 µM/side, dissolved in deionized water) alone and in combination. Control groups received either saline, deionized water, or DMSO. RESULTS: The H-89-treated animals showed significant increases in the time and distance travelled to find hidden platforms, and there was also a significant decrease in the time spent in the target quadrant compared to DMSO-treated animals. Nicotine and O-acetyl-L-carnitine had no significant effects on H-89-induced spatial learning impairments alone, but the bilateral intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevented H-89-induced spatial learning deficits and increased the time spent in the target quadrant in comparison with H-89-treated animals. CONCLUSIONS: Our results indicated the potential synergistic effects of nicotine and O-acetyl-L-carnitine in preventing protein kinase AII inhibitor (H-89)-induced spatial learning impairments.

An updated review of protective effects of rosemary and its active constituents against natural and chemical toxicities.

Natural and chemical toxic agents cause severe adverse effects on people's health in a variety of exposing ways. Herbal medications have taken into consideration as alternative safe treatments for toxicities. Rosmarinus officinalis also known as rosemary belongs to the Lamiaceae family. Rosemary and its constituents including carnosic acid, rosmarinic acid, and carnosol have a lot of benefits such as anti-inflammatory, antioxidant, anti-mutagenic, anti-bacterial, antiviral, antinociceptive, and neuroprotective activities. In this literate review, we focused on the protective effects of rosemary and its main compounds against natural and chemical toxicities in both in vitro and in vivo studies. The protective effects of rosemary and its components are mostly mediated through different mechanisms such as the inhibition of oxidative stress, reduction of inflammatory mediators including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-17 (IL-17), cyclooxygenase-2 (COX-2) and nuclear factor ĸB (NF-ĸB) as well as the modulation of apoptosis and mitogen-activated protein kinase (MAPK) signaling pathways.

Milk thistle (Silybum Marianum) as an antidote or a protective agent against natural or chemical toxicities: a review.

Biological and chemical agents cause dangerous effects on human health via different exposing ways. Recently, herbal medicine is considered as a biological and safe treatment for toxicities. Silybum marianum (milk thistle), belongs to the Asteraceae family, possesses different effects such as hepatoprotective, cardioprotective, neuroprotective, anti-inflammatory and anti-carcinogenic activities. Several studies have demonstrated that this plant has protective properties against toxic agents. Herein, the protective effects of S. marianum and its main component, silymarin, which is the mixture of flavonolignans including silibinin, silydianin and silychristin acts against different biological (mycotoxins, snake venoms, and bacterial toxins) and chemical (metals, fluoride, pesticides, cardiotoxic, neurotoxic, hepatotoxic, and nephrotoxic agents) poisons have been summarized. This review reveals that main protective effects of milk thistle and its components are attributed to radical scavenging, anti-oxidative, chelating, anti-apoptotic properties, and regulating the inflammatory responses.

Nigella sativa and thymoquinone attenuate oxidative stress and cognitive impairment following cerebral hypoperfusion in rats.

Nigella sativa, a plant widely used in traditional medicine, possesses anti-inflammatory, antioxidant and neuroprotective properties. In the present study, we investigated the effect of hydroalcoholic extract of N. sativa seeds (NSE) and its active constituent, thymoquinone (TQ), on learning and memory deficits, hippocampal acetylcholine esterase (AChE) activity, and markers of redox status, mainly lipid peroxidation and superoxide dismutase (SOD) activity following cerebral hypoperfusion in rats. Cerebral hypoperfusion was induced by permanent occlusion of bilateral common carotid arteries (2VO). Male Wistar rats were administered either a vehicle (sham group: 10 ml/kg/day, ip), NSE (100, 200, and 400 mg/kg/day, ip), TQ (10, 20, and 40 mg/kg/day, ip), or donepezil (5 mg/kg/day, ip) for 10 days (three days before and seven days after ligation). Spatial learning and memory deficits were investigated using the Morris water maze (MWM) task. 2VO produced significant learning and memory deficits as evidenced by increased latency time to reach the hidden platform, increased swimming time, and decreased time spent in the target quadrant in the probe trial in the MWM task. There was also a significant increase in the lipid peroxidation level and AChE activity, and a significant decrease in SOD activity in the hippocampal portion of hypoperfused rats, as compared with the sham group. Treatment with NSE (400 mg/kg/day; p < 0.001) and TQ (40 mg/kg/day; p < 0.001), as well as donepezil significantly prevented learning and memory impairments and alleviated changes in the hippocampal lipid peroxide level and SOD and AChE activities in this model. In conclusion, our data suggest that N. sativa and thymoquinone have a beneficial role in cerebrovascular insufficiency states and dementia.

Evaluation of Rheum Turkestanicum in Hexachlorobutadien-Induced Renal Toxicity.

Hexachlorobutadien is nephrotoxic agent in rodents. The mechanism of toxicity includes generation of free radicals, depletion of thiol groups and production of toxic metabolites. Antioxidant compounds may reduce HCBD-nephrotoxicity. In this research we investigated the effect of Rheum turkeatanicum extract against HCBD-toxicity. The animals were divided to 4 groups which were including control (saline, 1 mL/kg), HCBD (100 mg/kg) and treatment groups which received extract at doses 100 and 200 mg/kg. The extract were administered as intraperitoneally (i.p.) 1 h before HCBD injection (i.p.). The animals were anesthetized by ether, 24 h after HCBD administration. The results showed elevation of serum creatinine, serum urea, urinary protein, urinary glucose, malondialdehyde levels in kidney and reduction of thiol in kidney by HCBD. The histopathological studies showed that there was apoptosis and necrosis in HCBD treated groups. Administration of R.turkestanicum reduced HCBD toxicity. The extract reduced hitopathological changes in kidney. It may be concluded that the nephroprotective effect of extract may be due to different mechanisms such as antioxidant activity or by decreasing the toxic metabolites of HCBD or inhibition of enzymes which are involved in the bioactivation of HCBD such as glutathione-S-transferase (GST) or cysteine-S-conjugate ß-lyase.