In the last decade, many studies have shown that hydrogen gas or hydrogen water can reduce the levels of reactive oxygen species in the living body. Molecular hydrogen has antioxidant and antiapoptotic effects and a preventive effect on oxidative stress-induced cell death. In the present study, we investigated solidified hydrogen-occluding-silica (H₂-silica) that can release molecular hydrogen into cell culture medium because the use of hydrogen gas has strict handling limitations in hospital and medical facilities and laboratories, owing to its physicochemical characteristics. Human esophageal squamous cell carcinoma (KYSE-70) cells and normal human esophageal epithelial cells (HEEpiCs) were used to investigate the effects of H₂-silica on cell viability and proliferation. Cell migration was examined with wound healing and culture-insert migration assays. The intracellular levels of reactive oxygen species were evaluated with a nitroblue tetrazolium assay. To assess the apoptotic status of the cells, the Bax/Bcl-2 ratio and cleaved caspase-3 were analyzed by western blot. The results showed that KYSE-70 cells and HEEpiCs were generally inhibited by H₂-silica administration, and there was a significant proliferation-inhibitory effect in an H₂-silica concentration-dependent manner compared with the control group (P < 0.05) in KYSE-70. Apoptosis-inducing effect on KYSE-70 cells was observed in 10, 300, 600, and 1,200 ppm H₂-silica, and only 1,200 ppm H₂-silica caused a 2.4-fold increase in apoptosis in HEEpiCs compared with the control group as the index of Bax/Bcl-2. H₂ silica inhibited cell migration in KYSE-70 cells, and high concentrations had a cytotoxic effect on normal cells. These findings should provide insights into the mechanism of inhibition of H₂-silica on human cancer cells in vitro.

Postoperative pain is a common problem after inguinal herniotomy. We aimed to compare the intravenous anesthesia effects of propofol and isoflurane inhalation anesthesia on postoperative pain after inguinal herniotomy. In a randomized clinical trial, 102 eligible patients were selected based on inclusion and exclusion criteria and were randomly divided in two groups. In the first group, propofol was used for the maintenance of anesthesia, while isoflurane was used in the second group. The patient’s heart rate, systolic and diastolic blood pressure and oxygen saturation before, during and after surgery, recovery time and postoperative pain were measured immediately, 2, 4 and 6 hours after surgery and compared between two groups. T-test, and repeated measurement test were used for statistical analysis. No statistically significant differences were observed in heart rate, blood pressure and oxygen saturation levels between the two groups (P > 0.05). Propofol has higher effect in easing postoperative pain of patients than isoflurane, but no difference in postoperative complications, including chills, nausea and vomiting, occurs in both two groups. Propofol is effective in declining the postoperative pain of patients after anesthesia in comparison with isoflurane. Moreover, due to the antioxidant, anti-inflammatory and analgesic properties of propofol, it is preferred to isoflurane and the authors recommended it to be used.

Despite years of research, treatment of traumatic brain injury (TBI) remains challenging. Considerable data exists that some volatile anesthetics might be neuroprotective. However, several studies have also revealed a rather neurotoxic profile of anesthetics. In this study, we investigated the effects of argon 50%, desflurane 6% and their combination in an in vitro TBI model with incubation times similar to narcotic time slots in a daily clinical routine. Organotypic hippocampal brain slices of 5- to 7-day-old mice were cultivated for 14 days before TBI was performed. Slices were eventually incubated for 2 hours in an atmosphere containing no anesthetic gas, argon 50% or desflurane 6% or both. Trauma intensity was evaluated via fluorescent imagery. Our results show that neither argon 50% nor desflurane 6% nor their combination could significantly reduce the trauma intensity in comparison to the standard atmosphere. However, in comparison to desflurane 6%, argon 50% displayed a rather neuroprotective profile within the first 2 hours after a focal mechanical trauma (P = 0.015). A 2-hour incubation in an atmosphere containing both gases, argon 50% and desflurane 6%, did not result in significant effects in comparison to the argon 50% group or the desflurane 6% group. Our findings demonstrate that within a 2-hour incubation time neither argon nor desflurane could affect propidium iodide-detectable cell death in an in vitro TBI model in comparison to the standard atmosphere, although cell death was less with argon 50% than with desflurane 6%. The results show that within this short time period processes concerning the development of secondary injury are already taking place and may be manipulated by argon.

This study aimed to investigate the protective effects of hydrogen rich water on the intestinal ischemia/reperfusion (I/R) injury in a rat intestinal intussusception (II) model. Ninety Sprague-Dawley rats were randomly assigned into three groups (n = 30 per group). In sham group, rats received laparotomy, and the intestine was exposed for 15 minutes without II. In I/R + saline group and I/R + hydrogen group, rats received II after laparotomy and then intestine was relocated 8 hours later, followed by immediately intraperitoneal injection of normal saline and hydrogen rich water (HRW) (5 mL/kg), respectively. One hour later, the intestine was collected for hematoxylin-eosin staining and immunohistochemistry for apoptotic cells and 8-oxo-deoxyguanosine, and blood was harvested for detection of tumor necrosis factor-a, malondialdehyde and superoxide dismutase. Hematoxylin-eosin staining showed the intestinal mucosa was significantly damaged in I/R + saline group, which was markedly attenuated after HRW treatment. The serum tumor necrosis factor-α content increased significantly in I/R + saline group, but HRW treatment reduced serum tumor necrosis factor-α content as compared to I/R + saline group (P < 0.05). Serum malondialdehyde content and 8-oxo-deoxyguanosine positive cells in the intestine increased dramatically after II, but HRW significantly reduced them in I/R+hydrogen group (P < 0.05). In addition, superoxide dismutase activity reduced markedly and apoptotic cells increased in I/R + saline group as compared to sham group, but they HRW increased superoxide dismutase activity and reduced apoptotic cells significantly in I/R + hydrogen group (P < 0.05). Our results indicate hydrogen rich water is able to attenuate II induced intestinal I/R injury via inhibiting intestinal inflammation, attenuating intestinal/serum oxidative stress and reducing apoptotic intestinal cells.

Stroke is a cerebrovascular disease with high mortality and morbidity. Despite extensive research, there are only a very limited number of therapeutic approaches suitable for treatment of stroke patients as yet. Mounting evidence has demonstrated that such gases as oxygen, hydrogen and hydrogen sulfide are able to provide neuroprotection after stroke. In this paper, we will focus on the recent two years’ progress in the development of gas therapies of stroke and in understanding the molecular mechanisms underlying protection induced by medical gases. We will also discuss the advantages and challenges of these approaches and provide information for future study.

Hydrogen sulfide (H₂S) has been recognized and studied for nearly 300 years, but past researches mainly focus on its toxicity effect. During the past two decades, the majority of researches have reported that H₂S is a novel endogenous gaseous signal molecule in organisms, and play an important role in various systems and diseases. H₂S is mainly produced by three enzymes, including cystathionine β-synthase, cystathionine γ-lyase and 3-mercaptopyruvate sulfurtransferase along with cysteine aminotransferase. H₂S had been firstly reported as a neuromodulator in the brain, because of its essential role in the facilitating hippocampal long-term potentiation at physiological concentration. It is subsequently reported that H₂S may have relevance to neurologic disorders through antioxidative, anti-inflammatory, anti-apoptotic and additional effects. Recent basic medical studies and preclinical studies on neurologic diseases have demonstrated that the administration of H₂S at physiological or pharmacological levels attenuates brain injury. However, the neuroprotective effect of H₂S is concentration-dependent, only a comparatively low dose of H₂S can provide beneficial effect. Herein, we review the neuroprotevtive role of H₂S therapy in brain diseases from its mechanism to clinical application in animal and human subjects, and therefore provide the potential strategies for further clinical treatment.

As we all know, methane is a kind of fuel. Previous studies have shown that methanogens in the colon can react with carbon dioxide and hydrogen to produce methane. In a recent study, the anti-inflammatory effects of methane were shown in a dog model of small intestinal ischemia/reperfusion. The mechanism of this anti-inflammatory effect needs further investigation. Recently, studies have shown anti-inflammatory, anti-apoptotic and anti-oxidative effects of methane on different organic injuries. According to the results of these studies, we hypothesize that the initial effects of methane are to react with free radicals and enhance expression of antioxidase through forkhead box transcription factor class O pathway. The anti-inflammatory effect is following the anti-oxidative effect, and the anti-apoptotic effect relies on anti-inflammatory and anti-oxidative effects.

Helium has been classified as a kind of inert gas that is not effortless to spark chemical reactions with other substances in the past decades. Nevertheless, the cognition of scientists has gradually changed accompanied with a variety of studies revealing the potential molecular mechanism underlying organ-protection induced by helium. Especially, as a non-anesthetic gas which is deficient of relevant cardiopulmonary side effects, helium conditioning is recognized as an emerging and promising approach to exert favorable effects by mimicking the cardioprotection of anesthetic gases or xenon. In this review we will summarize advances in the underlying biological mechanisms and clinical applicability with regards to the cardioprotective effects of helium.

Spinal cord injury (SCI) is a complex disease process that involves both primary and secondary mechanisms of injury and can leave patients with devastating functional impairment as well as psychological debilitation. While no curative treatment is available for spinal cord injury, current therapeutic approaches focus on reducing the secondary injury that follows SCI. Hyperbaric oxygen (HBO) therapy has shown promising neuroprotective effects in several experimental studies, but the limited number of clinical reports have shown mixed findings. This review will provide an overview of the potential mechanisms by which HBO therapy may exert neuroprotection, provide a summary of the clinical application of HBO therapy in patients with SCI, and discuss avenues for future studies.

A 2-year-old girl experienced cardiac arrest after cold water drowning. Magnetic resonance imaging (MRI) showed deep gray matter injury on day 4 and cerebral atrophy with gray and white matter loss on day 32. Patient had no speech, gait, or responsiveness to commands on day 48 at hospital discharge. She received normobaric 100% oxygen treatment (2 L/minute for 45 minutes by nasal cannula, twice/day) since day 56 and then hyperbaric oxygen treatment (HBOT) at 1.3 atmosphere absolute (131.7 kPa) air/45 minutes, 5 days/week for 40 sessions since day 79; visually apparent and/or physical examination-documented neurological improvement occurred upon initiating each therapy. After HBOT, the patient had normal speech and cognition, assisted gait, residual fine motor and temperament deficits. MRI at 5 months after injury and 27 days after HBOT showed near-normalization of ventricles and reversal of atrophy. Subacute normobaric oxygen and HBOT were able to restore drowning-induced cortical gray matter and white matter loss, as documented by sequential MRI, and simultaneous neurological function, as documented by video and physical examinations.